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Emergency Medicine Core Training

Renal, Genitourinary, and Acid/Base Module


Welcome to the Renal, Genitourinary (GU), and Acid/Base module, part of the Emergency Medicine Core Training (EMCT) series. In this module, we will review the function of the renal system, disorders of the GU tract, and the pathophysiology and treatment of acid/base disorders. As in other EMCT modules, we will again help you build on your skills of developing differential diagnoses for various patient presentations. In the end, as usual, we will use scenario based learning to review presentations and managements of patient complaints related to our topics. For problems mimicking a renal and GU etiology, but are in fact are not, you will see links to other EMCT modules and may even see links to sources outside of this series for further descriptions.

Objectives of the Renal – Acid/Base module:

At the completion of this module, the student will be able to/better able to

  1. Describe the basic anatomy and physiology of the Renal system
  2. Describe how the body’s buffering system functions and how the kidneys help to maintain a stable pH
  3. Describe how the kidneys maintain a stable fluid and electrolyte balance in the body
  4. Describe the pathophysiologic processes and the treatment of various genito-urinary disorders
    1. UTI and Pyelonephritis
      1. Simple
      2. Complicated
    2. Male genital disorders
        1. Infections/STD’s
        2. Testicular torsion
        3. Epididymitis
        4. Cremasteric muscle strain
        5. Urethral foreign body
        6. Phimosis/paraphimosis
        7. Priapism
    3. Prostatic disorders
        1. BPH
        2. Urinary retention
        3. Prostate cancer
        4. Prostatitis
    4. Renal insufficiency and failure
        1. Acute
        2. Chronic
    5. Renal stone disease
    6. Dialysis complications
        1. Peritoneal
      1. Hemodialysis
    7. Acid-base disorders
    8. Renal toxins and therapies to avoid in cases of impaired renal function
  5. Describe the work-up, diagnosis, and management of various genito-urinary disorder scenarios
  6. Describe the work-up, diagnosis, and management of various conditions associated with renal failure
  7. Describe the work-up, diagnosis, and management of metabolic acidosis
          1. AGMA


With and without osmolal gap

          1. Non-AGMA
  1. Describe the work-up, diagnosis, and management of metabolic alkalosis


In order to maintain a healthy body, a state of homeostasis needs to exist. That requires a proper fluid balance, appropriate levels of various electrolytes, a stable pH, and good blood perfusion to tissues so nutrients can be delivered and wastes removed. The kidneys are integrally important in maintaining all of these homeostatic functions in the body, and dysfunction of this system can result in serious illness and even death. A normal pH of the blood is 7.40, and is maintained in a very tight range of +/- 0.05 of this value. A sustained pH of just +/- 0.25 outside of this normal range is incompatible with life, as cellular enzymes undergo conformational changes and fail to perform their usual functions of energy production and protein synthesis. A deviation in pH of greater than 0.5 will result in certain death unless corrected promptly. The kidneys have some ability to compensate for various metabolic and respiratory disorders, but understanding these disorders and how to assist in managing these is key to being a good provider. Before we jump into various pathophysiologic processes of GU and acid/base disorders, we will first start with an overview of clinically relevant anatomy and physiology.

Renal and GU Anatomy and Physiology:

The renal system is comprised of the body’s two kidneys and the structures dedicated to the excretion of urine: the ureters, urinary bladder and urethra. New figure 1


Figure 1

Structures of the urinary system

Used with permission of


Figure 2

Lateral vies of the structures of the male genital system and lower urinary tract

Used with permission of

The kidneys are not just filters for the blood, they do much more than produce urine as a waste product. The kidneys produce hormone and hormone-like substances such as erythropoietin, which stimulates red blood cell production in marrow, and renin, which helps to control blood pressure. These are discussed further in the endocrine module (link to endocrine A&P). Another major function of the kidneys is the production and excretion of bicarbonate, instrumental in maintaining a normal pH. The kidneys are also responsive to many drugs and hormones that influence fluid and electrolyte balance in the body.

The kidney is made up of an outer portion, the renal cortex and medulla, and an inner portion, the renal calyces and pelvis (Figure 3). Within the cortex, and extending into the medulla, are millions of nephrons (Figure 4a): blood filtering units that get rid of wastes, and regulate excretion and reabsorption of fluid and electrolytes. The waste ultimately becomes urine, and this is collected within the renal pelvis. It then travels through a tube (the ureter) to the urinary bladder, where it is ready to be expelled from the body. The kidney is the great regulator in the body in that it is capable of retaining more of a specific electrolyte when needed and getting rid of those that are not needed. When there are conditions of excess fluid (too much free water), the kidneys will expel hypotonic (dilute) urine. When there is a state of dehydration, the kidneys will retain fluid by reabsorbing sodium ions and will expel hypertonic urine which is concentrated mostly with wastes. Along with filtering then reabsorbing ions such as sodium (Na+), potassium (K+), and chloride (Cl), the kidneys also maintain acid/base balance by creating, reabsorbing, or excreting bicarbonate (HCO3) and hydrogen ions (H+).

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Figure 3

Internal anatomy of the kidney


Figure 4a

The nephron is the functional unit of the kidney. The glomerulus is a tuft of capillaries

that filters out wastes, electrolytes, and other plasma solutes into “Bowman’s Capsule.”

From here, these substances and water go through a process of reabsorption through various

tubules. In the end, wastes and any excesses are delivered to the collecting duct and

excreted in the urine.

The kidneys can control how much fluid is filtered through the glomerulus, the so called glomerular filtration rate (GFR), by controlling the hydrostatic pressure across this capillary bed. The glomerular capillary hydrostatic pressure is determined by how much blood flow is allowed in from the afferent arteriole and how much blood is allowed to flow out from the efferent arterial. This is one of the few areas in the body where capillaries have arteriole vessels on either side of a capillary bed. The illustration below, 4b, depicts how vasoconstriction and vasodilation of the afferent and efferent arterioles impact GFR. Certain hormones, such as B-Type Natriuretic Peptide (BNP), a variety of drugs, affect vascular tone of these arterioles and influence GFR.



Constricting the afferent arteriole and dilating the efferent arteriole will result in a decrease

in glomerular filtration rate (GFR). Dilating the afferent and constricting the efferent arteriole

will result in increased GFR, thus more filtrate will be sent to the renal tubules of the nephron,

and in turn, more urine produced.18

Body Fluids and Electrolytes:

The human body, on average, is made up of about 60% water (plus or minus depending on age, weight, and sex). Water is contained in two major “spaces” within the body: the intracellular space and extracellular space. About two thirds of the body’s fluid is contained within the confines of cell membranes. The fluid in the extracellular space is divided into two compartments: the intravascular space, which contains only about one quarter of the extracellular water, and the interstitial space. So, if a person weighs 70 kg, what we commonly refer to in medicine as the “average adult” (even though few people weigh 70 kg, as it is an average of male and female weights), then they will have about 42 kg (or liters) of water in their body. 28L of this water will be in the intracellular space, and the other 14 liters is in the extracellular space. Further, of that water in the extracellular (EC) space, 10.5L will be in the interstitial space and 3.5L will be in the intravascular space (Figure 5).

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Figure 5

Simple sketch illustrating the distribution of water into the various compartments or “spaces”

in the body. Two thirds of this volume will lie in the intracellular (IC) space, and one third will

lie in the extracellular (EC) space. Further, within the EC space, three quarters of this volume will

go to the interstitial (IS) space, and one quarter will go to the intravascular (IV) space.

Within each of these spaces are various concentrations of electrolytes (e.g. Na+, K+, Cl, HCO3), along with proteins, glucose, and other substances (Figure 6). Water flows freely between all of these compartments, as it follows the movement of particles. Particles will move between these spaces based on the influences of concentration and pressure gradients, their size and charge, and the accommodation of transport channels on the cell membrane.

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Figure 6

Normal distribution of the major particles in the intravascular (IVS), interstitial (ISS),

and intracellular (ICS) spaces. Electrolytes (Na+, K+, Cl, etc.) measured in meq/L.


Within the extracellular space, the primary cation is Na+ and the primary anions are Cl and HCO3. These particles flow quite freely between the intravascular and interstitial spaces based on concentration and pressure gradients (Figure 7: as discussed in the CV module). The cell membrane is a lipid, hydrophobic, barrier. Charged particles cannot cross this barrier without going through specialized pores or channels in the cell membrane. In this way, the intracellular environment can be, and is, vastly different than the extracellular milieu. The primary intracellular cation is K+, and the primary anions are organic phosphates and proteins. Much of the body’s energy (basal metabolism) is spent on maintaining this Na+/K+ gradient by way of providing ATP’s to the sodium/potassium pumps in the cell membrane.

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Figure 7

Two opposing forces affect the flow of fluid across the capillary membrane: hydrostatic pressure

and oncotic pressure. Hydrostatic pressure drops as the blood travels from the arteriolar end of the

capillary to the venule end. Oncotic pressure stays relatively the same. At the midportion of the

capillary, under normal conditions, there is equilibrium of pressures such that the only forces that

affect particle movement is concentration gradients. At the arteriolar end of the capillary hydrostatic

pressure is greater than oncotic pressure and fluid travels from the IVS to the ISS. At the venule end,

oncotic pressure from proteins in the plasma is greater than hydrostatic pressure and thus fluid is

drawn back into the intravascular space.

Acid /Base Physiology and the “Basic Chem Panel”:

Alright, take a deep breath because it is time for a review of some clinically relevant basic chemistry. Even if you were a chemistry major in college, I’m confident you will learn something useful here. For those that are a bit rusty with your chemistry, we’ll start with some of the basics.

If you look at a periodic table of elements (e.g. at, they are numbered according to how many protons, positively charged particles, they have their nucleus and organized into columns according to how they react. For example, the first column, on the left of the periodic table, starts with Hydrogen. Hydrogen has one proton in its nucleus, and, like all of the other elements in the first column, it has one electron in its outer “shell.” Without going into all of the theory behind this, just know that when there is only one electron in the outer shell, that element tends to “give up” that electron, when in solution, and become positively charged; in this case, it becomes a cation. So, elements from the first row that you will recognize in clinical medicine include hydrogen, lithium, sodium, and potassium, and these ionize into the following cations: H+, Li+, Na+, and K+. In the second column of the periodic table are at least 2 clinically relevant elements, magnesium and calcium, that have 2 electrons in their outer shell that are not tightly bonded to their nuclei, so they tend to give up both of these quite readily in solution, and become Mg2+ and Ca2+.

In order to give up these electrons and become positively charged, these cations have to give their electrons to other elements that want to “fill” their outer shells and accept an electron. These elements then become negatively charged particles in solution, or “anions.” In the last column of the periodic table are all of the elements that have their outer shell filled and are content just the way they are (the noble gases). In the second to the last column, are those elements that need one more electron to fill their outer shell: e.g. fluorine, chlorine, and iodine, which become fluoride (F), chloride (Cl), and iodide (I). Bicarbonate, HCO3, an organic buffer in the body, is another common anion. Proteins and organic phosphates (e.g. ATP) also have a net negative charge within their structure because they too accept electrons given up by the cations above. For every cation in solution there needs to be an anion, otherwise the solution would have some kind of charge, and that does not happen naturally.

An acid is a proton donor (H+ is simply a proton) and bases are molecules that accept protons. Strong acids essentially dissociate fully in solution, that is, the conjugate base steals the electron from hydrogen and H+ exists free in solution resulting in a maximal lowering of pH. Examples of strong acids you might encounter are hydrofluoric and hydrochloric acid: HF that dissociates into H+ and F, and HCl, that dissociates into H+ and Cl. Some acids are weak and dissociate only partially in solution. Many organic acids (those acids with a conjugate base that has a carbon atom in it) that you will encounter in the practice of emergency medicine, are moderately strong acids, such as lactic acid and ketoacids. pKa is a measure of the strength of an acid (a measure of how much it dissociates in solution). If the pKa is low, it dissociates very readily and is a strong acid. As the pKa approaches 7 (a neutral pH), it becomes a weaker and weaker acid.

The pH of a solution tells us whether it is acidic or basic. The pH of a solution is a measure of its acidity, and it is the activity, or concentration, of H+ in that solution that determines the pH. The human body, through normal metabolism, creates two substances that lead to elevated H+ concentrations: carbon dioxide (CO2), by the metabolism of carbohydrates and fats, and H+ directly, as a result of protein and fatty acid metabolism. Without some kind of buffering system in the body, there would be sudden massive drops in pH if we were to suddenly exert ourselves and create any amount of lactic acid. Bicarb, HCO3, is the major buffer of the body and exists at a concentration of around 25 meq/L. Hydrogen ions, (H+), normally exist at a concentration of about 40 nanoequivalents/L in serum, or a concentration that is roughly 650,000 times less than that of bicarb.3 Therefore, the body has a tremendous capacity to buffer acid production in the body, but as you will see in our scenarios, that capacity can become exhausted.

CO2 exists in three forms in the body: most as HCO3, more than 90%, and the rest as CO2 bound to hemoglobin, and CO2 as a gas dissolved in serum.5 An equilibrium exists between bicarb and CO2, and that is illustrated in the carbonic acid equilibrium equation:

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You will want to give special attention to this equation as it will help you to understand various acid/base disorders that are coming up. Notice that CO2 is a trapped gas in the body because of the residual volume of air in the lungs after every respiration. (link to A&P section of Resp module). If CO2 was not a “trapped gas” within the circulatory system, this equation would just go to completion to the right. Because of this trapped gas, we have an equilibrium between the trapped CO2 and bicarb. Carbonic acid, H2CO3, is simply an intermediary molecule and doesn’t really exist in any measurable concentration.

The normal pH of plasma in the human body is 7.40 (with a range of 7.35 – 7.45). The body maintains its pH within a very narrow range because of the complex buffering system that it has. Notice that conditions that move this equation to the right (e.g. hyperventilation, which releases more CO2 from the blood) will result in a decrease in H+ concentration as bicarb binds free H+, and an increase in pH results. Conditions that move the equation to the left (e.g. hypoventilation, which retains CO2 in the blood) results in an increase in H+ concentration, and a decrease in pH. This relationship is mathematically explained by the Henderson-Hasselbalch equation (pKa is a constant that varies with temperature, and for human physiology is 6.1). Without delving into this equation too far, simply note that pH ii inversely related to pCO2 and a proportionately related to HCO3.

There are 2 major systems at work to control pH in the body: the respiratory system and the renal system. The respiratory system influences the partial pressure of carbon dioxide (pCO2), and the renal system controls the concentrations of H+ and HCO3 in the serum. Disorders in acid/base, then, can result in acidosis or alkalosis. If the disorder is from a malfunction in the management of pCO2, it is referred to as a respiratory disorder, and if the disorder is a result of changes in concentration of H+ or HCO3, it is referred to as a metabolic disorder.

Laboratory Studies:

So, let’s move on to discuss those laboratory studies we obtain when we evaluate various metabolic and respiratory disorders. The basic chem panel provides a wealth of information as to the status of a patient’s metabolic and respiratory condition. Many abbreviations are used in medicine to expedite charting and the dissemination of information. With regard to electrolytes, a typical “panel” of labs include concentrations of sodium (Na+), potassium (K+), chloride (Cl), and bicarb (HCO3). In addition, this “chemistry panel” typically includes blood urea nitrogen (BUN), creatinine (a breakdown product of muscle), and glucose as well. Common shorthand for this panel is displayed below (Figure 8). Notice that the units are omitted because they are of a convention that is utilized widely in labs across the country (in the US that is, though different units and values are used in other parts of the world). For completeness, the approximate average normal values are listed first with their proper units, and then an example is displayed in the table below.

Na+ 140 mmol/L (or meq/L is used in some labs)

K+ 4.0 mmol/L

Cl 105 mmol/L

HCO3 25 mmol/L

BUN 14 mg/dL

Creat 1.0 mg/dL

Glucose 90 mg/dL

C:\Users\Steve\AppData\Local\Microsoft\Windows\INetCacheContent.Word\Renal fig 6.jpg

Figure 8

Shorthand for a basic chemistry panel

Another very useful test that is performed in order to assess acid/base status in the body is an arterial blood gas (ABG). A venous blood gas can be nearly as useful, but we will restrict our discussion to ABG’s at this time. An ABG blood sample is drawn from an easily accessible artery, commonly the radial artery at the level of the wrist, or in more extreme and difficult cases, the femoral artery via the groin. The first value of the ABG is the pH, and that is measured directly. The partial pressures of carbon dioxide and oxygen (in mmHg in the US, and in kPa in other parts of the world), are also measured directly from this sample. The bicarbonate concentration is also given as a reading on the ABG, but this is calculated via the Henderson-Hasselbalch equation (remember this from biochemistry?). The bicarb level will be similar to, but not necessarily the same as the bicarb level of the chem panel. This is because the chem panel is measuring all CO2 as it exists in the blood. Since more than 90% exists as bicarb, this is a good measure, but will slightly overestimate that actual amount of bicarb that exists in serum. The standard format for an ABG report is:


A typical normal ABG would be written as:


The normal values of an ABG with conventional units are:

pH 7.35 – 7.45

pCO2 38 – 42 mmHg

pO2 95 – 100 mmHg

HCO3 24 – 28 mmol/L (meq/L)

Genitourinary Disorders, Pathophysiology and Treatment:

Urinary Tract Infections (UTI’s):

UTI’s are the most common bacterial infection in humans, and occur about 30 times more frequently in women.7 They also tend to be recurrent. UTI’s typically start at the lower urinary tract, in the urethra and bladder, and work their way up the urinary tract, to the kidneys, when severe. Hematogenous spread of infection to the kidneys can also occur,7 but this mechanism of spread is much less common. UTI’s, then, can be separated into simple cystitis (inflammation of the urinary bladder) and pyelonephritis (inflammation from infection extending to the renal pelvis). Fecal bacteria colonize the perineum and can travel up the relatively short urethra of women, particularly after sexual intercourse, explaining the increase in prevalence of this infection in women. A rarer mechanism for UTI, that occurs almost exclusively in the elderly, is direct colonization of the urinary tract, typically the bladder, from adjacent bowel. This occurs in the case of an enterovesical fistula, in which case the bowel develops a fistulous communication with the urinary bladder and directly deposits wastes into the bladder: this can be a complication of diverticulitis.

All male urinary infections are “complicated” as they are unusual, unless some kind of instrumentation of the lower urinary tract has occurred. Other conditions that make a UTI complicated include the presence of diabetes, immunosuppression (e.g. from chemotherapy medications), pregnancy, and, of course, pyelonephritis, with associated fever. Structural abnormalities of the urinary tract, congenital or acquired, also make these infections complicated. In cases of complicated infection, the urine should be cultured so the offending organism can be cultured and appropriate treatment be assured. Untreated complicated urinary infections can result in renal injury or even failure.

The most common bacterial pathogen to cause simple cystitis in women is E. coli (about 85% of pathogens). A variety of other pathogens, essentially all fecal organisms, can also cause UTI’s, but less commonly. Treatment of acute cystitis should depend on local prevalence of various pathogens and antibiotic resistance, but first line therapy commonly includes Nitrofurantoin (100 mg bid X 5 days), TMP-SMX (160/800mg bid X 3 days), and Fosfomycin (3g sachet, single dose). Second line therapy includes Ciprofloxacin (250 mg bid X 3 days), Levofloxacin (250 or 500 mg qd X 3 days), Amoxicillin-clavulanate 500/125 mg bid X 7 days, and Cefpodoxime (100 mg bid X 3 -7 days).7 Phenazopyridine (Pyridium) can be used adjunctively for early symptomatic relief.


“Pyelo” is a urinary infection that involves the kidney, and specifically spreading into the renal pelvis and parenchyma (the functional and structural tissues of this organ).

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When a UTI progresses to the point of pyelonephritis, this is no longer a “simple” UTI. Young healthy women tend to recover from this infection quite readily and completely, whether a new or recurrent infection, but others can suffer the development severe renal impairment and even death. Causative organisms of acute pyelonephritis are, as in lower urinary tract infections, of bowel/fecal origin, with E. coli being, by far, the most common pathogen.  followed by Klebsiella (about 3 – 6% of cases), and others, including Proteus species.10 The most common mechanism for colonizing the kidney is via an ascending infection from a lower UTI, or cystitis. Hematogenous spread is possible, especially in cases of bacteremia/sepsis from another source, but this is rare.

Treatment of acute pyelonephritis depends largely on local resistance patterns of E. coli. In addition, taking into account how sick the patient is and whether this is a complicated infection or not will influence how aggressive the initial empiric treatment is. We will separate the treatment groups into those that can be treated as an outpatient, such as otherwise healthy women, and those that require hospitalization (have complicated infections).

Outpatient treatment for acute pyelonephritis can vary regionally, but a good regimen is:

Give an initial dose of ceftriaxone, one gram IV or IM, followed by ciprofloxacin 500 mg PO bid for 7 days. Levofloxacin 750 mg daily for 5 – 7 days can be substituted for cipro. Treatment can be modified at follow-up based on the results of the urine culture.11

Inpatient treatment for acute pyelonephritis depends on the severity of the illness and whether the patient appears septic. For non-septic patients, empiric treatment with a quinolone, such as ciprofloxacin 400 mg IV or Levofloxacin 500 mg IV, is appropriate. Ceftriaxone, 1 gram IV, is another good empiric treatment. For more extended coverage, piperacillin/tazobactam 3.375 g IV or meropenem 2 g IV can be given as the first dose of treatment. Again, treatment can be modified once the results of urine cultures return.11

Prostatic disorders:

Benign Prostatic Hyperplasia (BPH) is a commonly encountered disorder in the ED, generally manifested by urinary retention. Passing a urinary catheter in these patients and sending them on to a urologist (for further evaluation and management – including a work-up for cancer) is quite straight forward. Consider sending the patient out on an Alpha-1 receptor blocker (e.g. Tamsulosin) to “shrink” the prostate, by relaxing smooth muscle within the prostate and reversing hypertrophic changes.8

Prostatitis, in the acute phase, results when bacteria make their way into this organ and propagate. The prostate gland produces semen, which is essential for male reproductivity, and thus it has a contiguous connection to the urinary tract. In a manner similar to the mechanism of UTI’s, then, bacteria can colonize the prostate via direct communication with the urinary tract – by ascending through the urethra (most common mechanism), or via hematogenous or lymphatic spread. These infections tend to be recurrent and can lead to fever and even sepsis if treatment is delayed.

Treatment of acute bacterial prostatitis is directed at similar fecal pathogens that we see with acute cystitis and pyelonephritis, so many of these antibiotics will be the same. The difference in coverage, though, has to do with the antibiotic’s ability to penetrate deep into the tissues of the prostate, which requires a longer course of antibiotics as well. Standard, uncomplicated, treatment of acute prostatitis is a duration of 3 – 4 weeks with one of the following:9

  1. TMP/SMX DS, 1 tab bid
  2. Doxycycline, 100 mg bid
  3. Ciprofloxacin, 500 mg bid
  4. Norfloxacin, 400 mg bid
  5. Ofloxacin, 400 mg bid

Renal stone disease:

Renal stones, or calculi, are hard particles that form and enlarge in the kidneys. They are more common in men, with a life-time incidence of 12%, compared to women, life-time incidence of about 5%.12 Most calculi, about 80%, are “calcium stones,” composed of either calcium oxalate or calcium phosphate. The remaining stones are composed of struvite, uric acid, and rarely cystine.12 Stagnant or low flow of urine through the renal pelvis allows the dissolved calcium salts in the urine to aggregate into a solid state, and some have a hereditary propensity to be stone formers.12 Renal calculi can form anywhere there is stagnant urine along the urinary tract, even in the bladder, but they are most often found in the renal pelvis and calyces. It can be helpful in follow-up to analyze the stone after it is passed as there may be treatment to prevent formation of future stones.

Renal stones themselves are not much of a problem, but when they break loose from their position in the calyces or renal pelvis and obstruct the ureter, severe pain ensues as stretch receptors in the renal pelvis and ureter get stimulated.

Treatment of renal stones in the acute, emergent, setting revolves around making an accurate diagnosis and managing the patient’s pain, and the nausea that commonly accompanies this condition. Urologist will typically want to give these stones a chance to pass spontaneously, and many of these stones will pass without instrumentation. Have the patient strain all urine that is passed so the stone can be caught and its composition identified. There are some stones that are not likely to pass, and this is usually dependent on the size of the stone. Some patients have more difficulty passing stones than others, and a history of surgical extraction of ureteral calculi in the past makes it more likely that the patient will need surgical removal again. Some patients may require admission for pain control, but most will be able to be discharged, as long as early urology follow-up can be assured. One important factor to be cautious of is the presence of urine infection in the setting of an obstructing stone. If the patient has pyelonephritis and an obstructed ureter, this is a urologic emergency and the urologist should come to the ER to see the patient and arrange to have this obstruction relieved emergently.


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Figure ___

An illustration revealing a calculus obstructing the proximal ureter – at the ureteral pelvic

junction. This is causing marked hydronephrosis. Compare this to the normal kidney illustration

on the left.

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Figure ___

Coronal view of a CT scan of the Abdomen revealing left hydronephrosis. There is also an

incidental renal calculus in the lower pole, not currently causing pain or obstruction. Notice

the normal appearing renal pelvis in the right kidney.

C:\Users\Steve\AppData\Local\Microsoft\Windows\INetCache\Content.Word\Left UPJ calc.jpg

Figure ___

A large, 6 mm, ureteral calculus at the ureterovesical junction, causing left ureteral obstruction.

Male genital disorders: Male genital problems can present as lesions, masses, or pain.

Male genital lesions: If not traumatic, male genital lesions seen in emergency medicine are nearly always related to sexually transmitted diseases. These include…

Sexually transmitted diseases in men:

  • Gonorrhea: The second most common reported sexually transmitted disease, N. gonorrhoeae is the pathogenic organism of Gonorrhea.15 This is typically simply a urethritis in men, though it can go on to cause prostatitis. It also colonizes in the oral and conjunctival mucosa after exposure to someone with this infection.

The CDC recommends dual therapy for the treatment of uncomplicated Gonorrhea:15

    • ceftriaxone 250 mg IM along with azithromycin 1 g PO.
    • Alternative: Cefixime 400 mg PO plus azithromycin 1 g PO, each single dose

Treatment of Gonococcal conjunctivitis consists of ceftriaxone 1 g IM and azithromycin 1 g PO, each as single dose.

  • Chlamydia: This is the most common infectious disease, not just the most common STD, reported to the CDC. Prevalence is highest in the 24 or younger age group. Asymptomatic infection is common in both men and women but serious medical problems can result including PID and infertility, and can cause prostatitis in men. It is simply contracted through sexual activity with someone harboring this infection.16

Treatment of Chlamydia is most commonly accomplished with azithromycin 1g PO, single dose.

Alternate treatments include doxycycline 100mg PO bid for 7 days, or

Levofloxacin 500 mg PO for 7 days, or

Ofloxacin 300 mg bid for 7 days.16

  • Herpes Simplex: Genital herpes is caused by the herpes simplex virus and transmitted by intimate contact with another person with this infection: typically resulting in genital or oral ulcerative lesions. Though there are HSV-1 and HSV-2 infections, either can be the cause of genital or oral herpes. Fortunately, the treatment of both of these types is the same.

Treatment of first clinical episode of Herpes simplex17 is

acyclovir 400mg PO tid for 7-10 days or

Acyclovir 200mg PO 5 times per day for 7 – 10 days, or

Valacyclovir 1g PO bid for 7 – 10 days, or

Famciclovir 250mg PO tid for 7 – 10 days

  • Syphilis: Caused by Treponema pallidum, syphilis has been dubbed, the “Great Mimicker” because of the variety of ways in which it can present, many of which may suggest an alternate diagnosis.13 Remember to put this in your differential when patients are at risk for this infection. It can present in its primary form, as a painless ulcerative lesion on the genitals, in its secondary form, as a rash – most distinctively on the palms and soles – and mucocutaneous lesions, or in its tertiary form, with systemic involvement – particularly of the heart and brain. Latent syphilis is a term used to describe patients that are seropositive for syphilis but have no apparent clinical manifestations. Neurosyphilis is an infection of the brain and spinal cord that can result in cognitive, sensory, and motor dysfunction, and can result when syphilis has gone untreated for a decade or more.

The preferred treatment of syphilis, at all stages is, Penicillin G. Only the duration of therapy varies, as later stages of syphilis, especially latent syphilis, require longer courses of treatment.14

    • Primary and secondary syphilis:
      • Pen G 2.4 million units IM – single dose
      • Doxycycline 100 mg PO bid X14 days (for Pen allergic patients
    • Tertiary and Latent syphilis
      • Give Pen G 2.4 million units IM as first dose of treatment
      • The patient needs to follow-up for additional doses of Pen G to complete the course of treatment, up to 7.2 million units IM (three doses of 2.4 million units at weekly intervals

Remember, that sexual partners of all patients with the above STD’s should get treated. These infections should also get reported to your local department of health, and all of these patients should follow-up with their primary provider (or a local STD/communicable disease clinic)

  • There are other STD’s that you may encounter in emergency medicine, but they are much less common. If you encounter questions in this area, consult your emergency medicine specialist.

Epididymitis: Acute inflammation of the epididymis, acute epididymitis, is most commonly secondary to N. gonorrhea or C. trachomatis in the sexually male less than 35 years of age. The testicle is commonly involved in this infection as well: epididymo-orchitis. Sexually transmitted enteric organisms (e.g. E. coli and Pseudomonas species) can also cause this infection, from anal penetration. In the older population, bacteriuria from an obstructive uropathy, e.g. prostatic hypertrophy, is the most common cause of epididymitis.19

Treatment regimen for acute epididymitis is:

Ceftriaxone 250 mg IM plus Doxycycline 100 mg PO bid for 10 days

For acute epididymitis, likely due to an enteric organism:

Levofloxacin 500 mg PO daily for 10 days, or

Ofloxacin 300 mg PO bid for 10 days19

Note: high fever is uncommon in acute epididymitis. If a patient appears ill or has a high fever, admission to the hospital for IV antibiotics is recommended. If the patient has severe intractable pain, admission may also be warranted, but consider an alternate or comingled diagnosis such as testicular torsion.19

Testicular torsion: Testicular torsion is well recognized phenomenon and can result in loss of a testicle even with the rapid emergency department assessment. The timing of the evaluation and intervention will always be scrutinized when a bad outcome occurs. For this reason, acute testicular pain needs to receive a very high triage priority, and requires immediate evaluation by the provider.

Torsion of the testicle is fairly uncommon, occurring in about 1 in 4,000 males under the age of 25, but can occur in all ages. It is most often related to an anatomic predisposition some males have, a so called, “bell clapper” deformity, where there is a lack of connective tissue in the scrotum securing the testicle to the inner wall of the scrotum.20 It can come with activity or even during sleep.

Treatment of testicular torsion is always surgical ultimately, for exploration, detorsion, and orchiopexy (securing the testicle to the inner scrotal wall). It has been found, though, that manual detorsion. in the emergency department, ahead of surgery has been found to improve outcome in these patients.21 Because most cases of torsion result from lateral to medial movement of the testicle, it tends to rotate to the middle with the right testicle rotating clockwise and the left rotating counterclockwise.22 For this reason, using the “opening the book” technique of reversing testicular torsion is most common empiric manual treatment: i.e. the right testicle is rotated counterclockwise and the left testicle is rotated clockwise. 2 caveats here: 1) you must be certain of your diagnosis ahead of performing this procedure so as not to inflict torsion of a testicle on a patient that already has testicular pain from another cause, and 2) this procedure will require pain control and sedation ahead of performing it because most males won’t let you near their testicles while experiencing this excruciating pain.

Epididymal and testicular appendix torsion: Most emergency providers lump these two similar diagnoses into one category since their presentation, clinical course, treatment, and outcome are essentially the same. For that reason, we will do that too. For academic reasons, this illustration depicts the difference.

C:\Users\Steve\AppData\Local\Microsoft\Windows\INetCache\Content.Word\torsed appendage testis vs torseed appendage epididymis.gif

Figure ___

This illustration demonstrates the two types of torsion appendices that cause scrotal

pain, torsion of the appendix testis and torsion of the appendix epididymis.

Remake this figure

“Torsion of the testicular appendix is the commonest cause of acute scrotal pain in children.”23 Both testicular and epidydimal appendices are embryologic vestiges that serve no known purpose and are located at the superior aspect of the testicle. This is a benign condition, but causes severe pain and can mimic testicular torsion clinically.

Treatment of acute appendix torsion is pain control, but this requires an accurate diagnosis. A classic “blue dot sign” may be seen and palpated clinically, in both appendix testis and appendix epididymis torsion, as a nodule on the superior aspect of the testicle, but ultrasound is the diagnostic modality of choice for affirming the presence of torsion of the epididymal appendix.24 Getting a classic finding on ultrasound for this condition can avoid unnecessary surgery and unnecessary antibiotics.

Cremasteric muscle strain: A benign cause of scrotal pain that can mimic torsion is strain of the muscles that elevate the testicles in the setting of exposure to a cold environment. This can occur in joggers that run in very cold weather proper scrotal support can result in stretching of the cremasteric muscle as it attempts to draw the testicle closer to the warm body of the jogger. On exam, the patient will want you to avoid touching their scrotum. The testicles will tend to be positioned high in the scrotum. It will be difficult to determine if this is epididymitis or cremasteric strain, and torsion will still be in the differential. The onset will commonly be indolent, over several hours, so getting a scrotal US to rule-out torsion and epididymitis is appropriate. Cremasteric muscle strain is a diagnosis of exclusion and is based on appropriate history

Treatment of cremasteric muscle strain is simple pain control. Non-steroidal anti-inflammatories are the best option for otherwise young and healthy males, but a short course of opiates may be necessary in some patients with more severe pain.

Priapism: Priapism is a persistent, unstimulated, erection that lasts for hours, and typically only involves the corpora cavernosa. Certain drugs, including trazodone and thorazine, can cause this condition.

Priapism can be one of three types:

  1. Ischemic: a veno-occlusive mechanism. There is little or no cavernous blood flow, and this blood is hypoxic, hypercarbic, and acidotic. The corpora cavernosa are rigid and tender, and the patient typically reports pain.
  2. Nonischemic: a high arterial flow mechanism. The persistent erection is due to unregulated and excessive arterial inflow to the corpora cavernosa. Cavernosal blood gasses in this case are not hypoxic or acidotic. The penis is not typically as rigid or tender, as it is in ischemic priapism.
  3. Stuttering or intermittent: recurrent paroxysms of ischemic priapism with intervals of detumescence in between.

Priapism is a relatively uncommon condition, but can be a medical emergency as the patient with ischemic priapism can suffer fibrosis of the cavernosal tissues and develop permanent erectile dysfunction. Early intervention to achieve detumescence is the goal, but even these therapies can be harmful and result in erectile dysfunction.25

Treatment needs to be prompt in cases of ischemic priapism and though there are invasive emergent diagnostic and therapeutic options, the new provider should simply seek emergent urologic consultation when faced with a case that could be ischemic priapism. It may be appropriate to try some interventions, such as intracavernous injections of phenylephrine, but if this patient has sickle cell disease or an underlying hematologic malignancy, systemic treatment alone is not likely to be helpful and early evaluation by a urologist and surgical intervention should be pursued.25 Bottom line, a painful and tender penile erection persisting for 4 hours warrants a call to the urologist and an emergent evaluation and intervention.

Penile fracture: The corpora cavernosa is covered by a fibrous layer of tissue, the tunica albuginea. If the penis is suddenly bent or torqued to a critical angle, this fibrous covering can split and hemorrhage from the corpora can be released under the skin. This is not a diagnostic dilemma, and the treatment is urological consultation.

Phimosis/paraphimosis, Balanitis and Posthitis: Phimosis is a generally a benign condition, and is seldom seen in the ER. It is a condition in which the foreskin, prepuce, cannot be retracted over the head, or glans, of the penis. In severe cases, it may lead to difficulty passing urine. In children, it can be difficult to retract the prepuce of a non-circumcised male, and this is common and expected as 96% of males have nonretractable foreskin at birth.26 As the boy gets older, it becomes easier to retract the prepuce. Pediatricians and family physicians usually manage this condition, and referral to a urologist is generally not necessary. Aggressive attempts at retracting the foreskin can lead to local minor trauma and breaks in the skin, setting the stage for infection. Not keeping the area clean and not retracting the foreskin as an adult can lead to overgrowth of fungi, such as candida, and mixed bacterial species, such as Gardnerella vaginalis. This can lead to balanitis (infection of the glans penis) and/or posthitis (infection of the foreskin). Commonly local cleansing and topical antifungals are sufficient, but in severe cases, with tender edema of the glans or induration of the foreskin, oral antibiotics may be cover skin flora (Staph and Strep) as well has some bowel related flora and STD’s.27

Paraphimosis is a much more concerning condition. In this case, the retracted foreskin of the uncircumcised male gets retracted, but is not able to be returned to its normal position. As it stays in this position, the prepuce can become edematous making circulation to the glans more tenuous. At the same time, venous and lymphatic return from the glans is impaired, so the head of the penis begins to swell, as arterial circulation to the glans is under higher pressure and is less restricted. This can result in severe ischemia or even necrosis of the glans.

Treatment of paraphimosis needs to be urgent in order to prevent, or at least mitigate, long term complications of this problem. Because of the swelling, this is commonly very painful for the patient. Administering a pain medication, commonly an opiate parenterally, or utilizing sedation medications, such as ketamine or nitrous gas, should be one of your first steps, as this becomes a very painful condition. Placing a copious amount of viscous lidocaine over the end of the penis will help with manual reduction and provide some additional pain control. Allow this to absorb over a period of about 10 minutes. An ice pack can also be applied during this time. The next step is to manual reduction. Firmly squeeze the end of the penis with your hand to reduce the swelling the retracted prepuce and glans of penis. This may take an extended period of time.28 Eventually, the swelling will generally subside sufficiently so you can bring the prepuce over the head of the penis again. Good perfusion should be apparent and the patient’s pain should be resolved. If this is not successful, call for immediate urologic consultation, as, in worst case scenario, an emergent circumcision may need to be performed. Do not attempt reduction if necrosis of the glans is apparent or if there are signs of significant infection. Call the urologist immediately.

Rhabdomyolysis: Rhabdomyolysis, or “Rhabdo,” is a condition that results from the injury of skeletal muscle tissue and the subsequent release of its contents into the extracellular space (first to the interstitial then the intravascular space). One of the products released from these damaged muscle cells is myoglobin, which filters through the glomeruli and ultimately plugs renal tubules leading to renal insufficiency and even failure, and creatinine phosphokinase, known as CK or CPK for short.29 It is the latter that we generally measure to determine the degree of severity of the rhabdo and it is used to guide treatment.

Muscle injury leading to rhabdomyolysis can be from something as simple as over use of muscles, example after running a marathon, or something as serious as a crush injury leading to direct muscle trauma or a secondary compartment syndrome leading to necrosis of muscle as a result of hypoperfusion. Certain drugs, such as amphetamine agents and MDMA and agents predisposing to serotonin syndrome, can lead to agitation and hyperthermia and muscle breakdown. Electrical injuries, infection, and certain metabolic conditions can also lead to this disorder.29 Rhabdomyolysis is generally defined as a CPK level greater than 1,000 U/L.

Treatment of mild rhabdomyolysis is to first eliminate the underlying cause, if that is still going on. This may require sedation and even chemical paralysis for the agitated patient. Simple normal saline fluid resuscitation may be sufficient for mild cases of rhabdomyolysis, but as CPK levels approach 10,000 U/L, and definitely when they approach 100,000 U/L or more, giving large volume of a buffered crystalloid solution is necessary. Put 2 amps, 100 mL (100 mmol), of bicarb into a bag of 5% dextrose solution (D5W). Immediately administer 2 liters to the average adult, and let urine output (from a urinary catheter) guide management from there. Talk to your local EM specialist about further management as these patients may require up to 10L of fluid or more early on to mitigate renal injury.29 Monitoring CPK levels can be a useful guide to therapy for prolonged stays in the ER, and in the case of mild CPK elevations, less than 10,000, from something like physical exertion from a marathon, observing the patient in the ER as they get hydrated and discharge is appropriate if the CPK is trending down toward a normal level. Early follow-up should always be stressed.

Renal insufficiency and failure:

Patients with end-stage renal disease are some of the most vulnerable patients you will care for, when it comes to risk of serious infections, metabolic disorders, and cardiopulmonary disorders. Renal failure is also commonly associated with hypertension, diabetes mellitus, and vascular disease. Simply managing these patients on a case-by-case basis, guided by their clinical presentation, is all that can be recommended, but keep in mind that sepsis, MI, acidosis, and other serious disorders can be occult until the patient suddenly experiences cardiopulmonary collapse.

Recognizing patients with mild renal insufficiency are a special at-risk population. Use caution when prescribing medications that may worsen renal injury, e.g. NSAID’s and sulfa meds, and when ordering tests that require administration of contrast. The variety of presentations in this condition are too broad to address comprehensively. Talk to your EM specialist early when confronted with difficult cases.

Dialysis Complications: Patients can develop end-stage renal disease acutely, from causes such as sepsis, toxins, or adverse medication effects, or from chronic disease, such as diabetes and hypertension. When acute renal failure occurs, patients are typically placed initially on hemodialysis. The patient’s blood is filtered through the dialyzer by way of a large bore, two port, central line (commonly placed in the subclavian vein). In renal failure is more indolent, the nephrologist has time to prepare the patient for dialysis, and a preference for hemodialysis (HD) or peritoneal dialysis (PD) can be determined, while going through the process of candidacy for renal transplant. PD requires placement of a transcutaneous catheter into the open abdominal cavity and long-term HD requires surgical creation of an arterial-venous fistula, typically in the forearm where there is redundant arterial circulation.

The most common emergency complication of hemodialysis is fluid overload with shortness of breath and pulmonary edema, commonly due to a missed run. It is a difficult balance for the nephrology team to get the patient to an adequate “dry weight,” yet avoid making them hypotensive with postural changes. For patients, strict adherence to fluid and sodium restrictions must be followed, and this isn’t always the case.30 Patients will most commonly present fluid overloaded and hypertensive, with feelings of shortness of breath. They may present in extremis, coughing frothy sputum and exhibiting signs of fulminant pulmonary edema.

Treatment of fluid overload in the dialysis patient: In patients that are entirely anuric, following the usual routine of giving diuretics will be mostly futile. For patients that still produce some urine, giving high dose diuretics, e.g. 80 to 160 mg furosemide IV, is reasonable. In addition, though, decreasing afterload will be key to decreasing pulmonary congestion. Placing the patient on a nitroglycerine drip, starting at 5 to 10 mcg/min and titrating to 60 mcg/min as needed, or nitroprusside, starting at _____ and titrating to ____, would be the best approach. Acute myocardial infarction can also be a cause of sudden pulmonary edema in the dialysis patient, so this should always be looked for. Dialysis patients are also very susceptible to various infectious processes, so consideration of pneumonia in hypoxic/dyspneic dialysis patients is also very important. Of course, immediate consultation with a nephrologist is paramount as you consider acute hemodialysis for these patients.

Hyperkalemia in the dialysis patient: In addition to fluid overload, dialysis patients are prone to electrolyte abnormalities, most notably hyperkalemia. After all, without adequate kidney function, the only way to regulate total body electrolytes is to monitor what is taken out with dialysis and what is put in via diet. Hyperkalemia causes the resting potential to be raised, making the cardiac muscle more “irritable,” and more likely to propagate signals. This leads to cardiac conductive abnormalities with widening of the QRS complex. Ultimately, a classic sinusoidal rhythm results and the patient goes into full cardiac arrest.

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Figure ___

Severely hyperkalemic hemodialysis patient with profound widening of the QRS complex.

This is near to the classic sinusoidal rhythm that immediately precedes cardiovascular collapse.

Treatment of hyperkalemia in the dialysis patient: Conventional acute treatment for hyperkalemia in the dialysis patient is generally same as it is with patients with normal renal function, as the goal is the same: move K+ to the intracellular environment and stabilize the cell membrane of cardiac conductive tissues. These medical treatments are temporizing, and life-saving, measures used to bridge the patient until dialysis can be performed. To accomplish this, the first medication to administer is Calcium gluconate, 1 amp IV, to stabilize cardiac cell membranes.

The next most important drug is insulin: 10U regular insulin IV to the average adult. Independent of its effects on glucose transport into cells, it stimulates the Na+/K+ ATPase pump on cell membranes, which results in greater movement of K+ to the intracellular environment. Give an amp of D50 to normoglycemic patients to prevent a hypoglycemic reaction.

Albuterol, administered IV, or most commonly via continuous nebulization (up to 10 to 20 mg), also has an adjunctive effect on reducing serum K+ levels: by stimulating action of the Na+/K+ ATPase pump.

Bicarb to prevent, or correct, acidemia is important, as acidemia causes mobilization of K+ from the cell, as H+ moves to the intracellular environment to balance the pH. The routine use of bicarb in all hyperkalemic patients, though, is controversial.32 When used, administering 1 amp of bicarb at a time is appropriate, then watch for the desired effect (correction of acidosis).

Diuretics, such as furosemide bumetanide, can be used in patients with at least some urine output. Administering normal saline boluses, 1 to 2 liters, to non-renal failure patients along with diuretics (even as little as 20 mg of furosemide IV push can be used in patients that have never used this drug and have good renal function, or 40 – 80 mg IV to patients with impaired renal function or those on this medication already) will result in a net increase urine potassium excretion. Having a urinary catheter placed can help to track urine output and guide therapy.

Cation-exchange resins, e.g. Kayexalate, used to be a common adjunctive treatment for removing potassium from the body of hyperkalemic patients, but serious problems have been recognized over the past several years and this therapy is no longer recommended. These exchange resins were not found to be very effective in the first place, and when it was discovered that they could cause colonic necrosis and increased morbidity and mortality in patients, its usefulness was no longer justified.33 Bottom line: do not use cation-exchange resins.

C:\Users\Steve\AppData\Local\Microsoft\Windows\INetCache\Content.Word\severe hyperK+ post tx - JA.JPG

Figure ___

Same hemodialysis patient as above after medical treatment, still awaiting an emergent HD run.

Notice that the QRS is greatly narrowed, but there is still a widened terminal S-wave. This patient

Is not yet “out of the woods,” and is still in need of emergent dialysis.

Other complications of hemodialysis include, bleeding at puncture site of graft, particularly in anticoagulated patients. Direct pressure is usually all that is necessary, but patients have commonly exhausted this option by the time they come to the ED and surgical consultation may be required in extreme cases.

The dialysis complication most common and most unique to peritoneal dialysis patients is acute bacterial peritonitis.31 Seeding of bacteria to the peritoneal space is easy to do with all of the exchanges of fluid that take place on a daily basis through the PD catheter. Abdominal pain and fever are early manifestations of this problem, and quick diagnosis and treatment is needed for a good outcome. Discuss treatment options with your nephrology specialist.

All dialysis patients are extremely prone to various infections, and these need to be individualized. Any dialysis patient with even a low-grade fever, should be rapidly screened for sepsis. Consult your emergency medicine or nephrology specialist early when managing this sick population of patients.

Renal Transplant Patients:

Renal transplant patients can present to the ED with minor medical issues and trauma just like any other patients, and simply addressing these issues are fine if that is all that is going on. When presenting with fever, or even vague symptoms, such as fatigue or diffuse body aches, they need to be treated like any other immunosuppressed patient presenting to the ED: they can quickly develop overwhelming sepsis. These patients also commonly have significant risk factors for coronary disease and other vascular disease. In addition, stability of renal function needs to be determined early to rule out acute renal injury or graft rejection. Perform a thorough evaluation of these patients, and because of their complexity, early consultation with an emergency specialist, via telemedicine if needed, is recommended, depending on your comfort with the patient’s condition.

Electrolyte Disorders, Pathophysiology and Treatment:

Common electrolyte disorders include the following:

Hyponatremia: Hyponatremia is commonly discovered abnormality on lab tests, and is defined as a sodium level less than 135 mmol/L. If the patient is euvolemic (has normal blood volume) or hypervolemic (excess body fluid with edema present), there is probably a normal total body sodium load. If the patient is hypovolemic (showing signs of dehydration), then there is a total body deficit of sodium in this hyponatremic population.

Many drugs and conditions can cause hyponatremia. Diuretics in the elderly are notorious for causing hyponatremia, and this may be necessary chronically in CHF patients in order to keep total body water down. Several psychiatric drugs, such as chlorpromazine and SSRI’s (selective serotonin reuptake inhibitors), along with many other drugs and cause the body to lose sodium from the kidneys. SIADH (syndrome of inappropriate antidiuretic hormone) is a condition where the body loses control of the production and release of ADH (it can be produced by certain tumors. This results in retention of free water and hyponatremia. Psychogenic polydipsia is the excess drinking of water that some schizophrenic patients do, and acutely, can drink to the point of passing out. A common, unintended, form of hyponatremia occurs when a patient that is vomiting gets dehydrated, then replaces body fluid loss simply with free water (not taking in electrolytes orally). The body cannot excrete just free water in the urine, so, though dilute, still has to give up some sodium.

Hyponatremia can have dire consequences with the Na+ level gets to 125 mmol/L or less, as seizures can occur and can become intractable.

Treatment of acute or chronic hyponatremia should not be carried out too fast, though in extreme cases, as in the patient seizing due to hyponatremia, hypertonic (3%) saline can be given, but the goal is still only to raise the 1 to 2 mmol/L per hour.34 In most cases, if hyponatremia needs to be treated and isn’t simply chronic (e.g. at a level of 130 mmol/L), giving normal saline (0.9%) boluses are generally sufficient. This will avoid complications of brain injury that can happen when correcting serum sodium levels too rapidly with 3% saline. If you are looking to use 3% saline, this would be a good time to contact your emergency medicine or internal medicine specialist.

Hypernatremia: Hypernatremia is defined as a level above the normal range of serum sodium, i.e. greater than 145 mmol/L. This is typically caused by total body loss, and results as your body attempts to hang on to Na+ in an effort to reabsorb more fluid from the renal tubules. Hypernatremic patients will be hyperosmolar as well, and since N+ is primarily extracellular, this will result in fluid leaving the cells. In the brain, this results in confusion and change in mental status, and ultimately leads to coma.

Treatment of hypernatremia is with normal saline. Correcting the Na+ level too fast, particularly if using a hypotonic solution, such as D5W or even “half” (0.45%) normal saline, will result in cerebral edema, as the shrunken brain cells that are suddenly hypertonic compared to the extracellular space take in water.

Hypokalemia: Low K+ is another common finding on labs and is defined as a serum level less than 3.5 mmol/L. As K+ levels approach 2.5 mmol/L or less, serious adverse events can occur, including dysrhythmias and sudden cardiac death. Mild hypokalemia may simply manifest as generalized weakness and fatigue or GI symptoms due to slowed motility. This can be due to diuretic use or from simply drinking free water when thirsty, or other non-potassium containing drinks or food. Vomiting and diarrhea can result in K+ loss as well.

Treatment of hypokalemia can be with oral potassium chloride tablets, or sequential “bumps” of IV potassium in more severe cases. When giving K+ IV, the patient needs to be on a cardiac monitored so any dysrhythmias can be detected, and it should be given slowly: 10 meq over 30 to 60 minutes.

Hyperkalemia: Hyperkalemia has already been discussed in the renal failure section. Remember to treat this early and aggressively, and in patients with normal renal function, giving normal saline fluid boluses along with diuretics can induce the kidneys to clear excess K+. In severe cases, the ultimate treatment is dialysis so, discuss this patient with your closest on-call nephrologist.

Hypocalcemia: Low calcium, defined as an ionized Ca2+ level of less than 2.1 mmol/L, is typically the result of a hormonal problem in the body (regulated largely by the parathyroid gland) and is commonly a mild, chronic problem that we will not deal with in the emergency department. If the Ca2+ is profoundly low, ionized calcium of less than 1 mmol/L, or the patient is symptomatic (experiencing paresthesia, muscle cramps/spasms, tetany, seizures), giving 1 to 2 amps of calcium gluconate through an adequate venous line (preferably a central line) over 5 – 10 minutes would be indicated.35 Contact your emergency medicine or internal medicine specialist if you have questions regarding treatment of hypocalcemia at home. If discharged, all of these patients require early follow-up.

Hypercalcemia: Hypercalcemia is generally reported in terms of “total plasma calcium levels” as opposed to ionized Ca2+ levels. The normal total plasma calcium level range is 8.5 to 10.5 mg/dL (varies slightly with age).. Like hypocalcemia, this is generally a chronic, mild, problem and not something we correct, or even address, in the emergency department. This is commonly a hormonal condition, but can be from lytic lesions in bone. In cases of extreme hypercalcemia, and in those that are symptomatic (cognitive dysfunction, fatigue, shortened QT on ECG, muscle weakness/aches), acute treatment and admission to the hospital may be necessary.36 The work-up for a cause, in these cases, can be part of the admission.

All patients with a total serum Ca2+ level of greater than 14 mg/dL, and all symptomatic patients with a serum Ca2+ greater than 12 mg/dL, should be aggressively treated for their hypercalcemia. The goal of this emergent therapy is to increase renal excretion of Ca2+. Hydrate the patient with 1 to 2 liters of normal saline over an hour, then administer a loop diuretic, such as furosemide 20 – 40 mg IV, and monitor urine output. Monitor potassium and magnesium levels and replace as needed.36 Admit these patients to the hospital for further treatment and monitoring. For renal failure patients, contact your local nephrologist to discuss dialysis.

Hypomagnesemia: Only 0.3% of the body’s magnesium is found in plasma (65% is contained in bone), so the serum level is not a very good predictor of total body Mg2+. The normal serum Mg2+ level is held in a very tight range, from 1.5 – 1.9 meq/L (or 0.75 – 0.95 mmol/L, or 1.7 – 2.2 mg/dL): your lab will likely use units of mg/dL. The kidneys play a crucial role in electrolyte homeostasis, including regulating Mg2+ levels, but oral intake is also important. Chronic alcoholics, patients with diarrhea, those found to be hypokalemic or hypocalcemic, and those with cardiac dysrhythmias or muscle weakness should have a Mg2+ level checked.

The treatment of hypomagnesemia is the administration of magnesium sulfate: 2 g in 100 ml D5W IV over 5-10 minutes. Patents with a Mg2+ level of less than 1.2 mg/dL (or 1 meq/L) should be given supplemental magnesium.37

Acid/Base Disorders, Pathophysiology and Treatment:

There are 4 basic acid/base disorders: 2 metabolic disorders (metabolic acidosis and alkalosis) and 2 respiratory disorders (respiratory acidosis and alkalosis). These disorders can, for the most part, be explained by the using the carbonic acid equation:

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Disorders that move the carbonic acid equation to the left, or result in greater H+ concentrations, cause acidosis. The converse is true, in that disorders that move the equation to the right, or result in a lesser H+ concentration, cause alkalosis. The exception to this rule: Drinking lots of water (adding substrate to the right side of the equation) does not result in any significant change in pH. Also note that in metabolic acidosis, H+ is produced which binds to HCO3 as it is neutralized. This would result in an accumulation of CO2 in the blood. Fortunately, the body senses this and will normally respond by hyperventilating in a state of metabolic acidosis, thus facilitating the binding of HCO3 to H+ and will compensate for this acidosis. Each Acid/Base disorder will be discussed individually.

Respiratory acidosis:

Respiratory acidosis results from an excess of CO2 in the serum. This typically occurs because normal air exchange is impaired at the level of the alveoli. Causes may be that the patient’s ventilations are suppressed, as can be the case with an opiate overdose, or that there is airway obstruction impeding adequate flow of air in and out of the alveoli, as can be the case with asthma or emphysema. The end result is a rise in pCO2 in the alveolus, which leads to a rise in serum pCO2, and this condition results in an increase in [H+] (hydrogen ion concentration) and decrease in pH.

Treatment of respiratory acidosis is directed at the underlying cause of this condition, including endotracheal intubation, naloxone for opiate overdoses, bronchodilators for bronchospasm, BiPAP, and more. Refer to Respiratory module for more details regarding the management of respiratory failure. (link to Resp failure section of Resp module)

Respiratory Alkalosis:

Respiratory alkalosis results from a decrease in CO2 in the serum. This typically occurs as a result of hyperventilation and the resulting increase gas exchange with the environment. pCO2 in the alveolus promptly drops to less than 40 mmHg, and then rapidly equilibrates with the alveolar capillaries and draws increased CO2 from the serum causing the serum pCO2 to go down. The carbonic acid equation moves to the right, as H+ binds with HCO3, and alkalosis ensues. Conditions that can cause hyperventilation are acute anxiety (panic attacks) and reactions to certain drugs (e.g. early reaction to aspirin overdose). Patients may also compensate for a metabolic acidosis by hyperventilating, but not to a point that there pH will go to a level greater than 7.35, so they will remain acidotic.

Treatment of respiratory alkalosis is directed at the underlying cause. Please refer to the Respiratory module for more details of the management of this condition. (link to resp alkalosis section of resp module)

Metabolic Acidosis:

Metabolic acidosis is the most complex acid/base disorder because there are so many causes for this condition. This is also an important topic because it is a common disorder and can occur in many different situations. In short, anytime there is a condition that results in excess acid production, increased H+ reabsorption (from the kidneys), decreased HCO3 production, or increased utilization or excretion (from the kidneys) of HCO3, the result is a metabolic acidosis. Because there are so many different causes of metabolic acidosis, we must break them into categories of anion gap and non-anion gap etiologies.

Anion Gap:

An “anion gap” (AG) implies that there is an anion (negatively charged particle) in the serum that is not accounted for. Basic chemistry tells us that a solution must exhibit electrical neutrality. That is to say that the number of charges of cations in the serum must be equivalent to the number of charges of the anions. Since the primary cation in serum is Na+(sodium), and the primary anions are Cl and HCO3, an equation can be written to show a balance between these charged particles:

AG = [Na+] – [Cl] – [HCO3]

K+ can be added to this equation as well, but it is usually ignored since its concentration does not change appreciably, even in extreme cases, and its concentration is relatively small. Under normal circumstances, the [Na+] is about 140 mmol/L, the [Cl] is about 105 mmol/L, and the [HCO3 ] is about 25 mmol/L. In this case, the anion gap would be 10. A normal AG is anywhere from 8 – 16 mmol/L (or more appropriately, meq/L). Given the example then, this means that, under normal conditions, proteins and other trace anions in the serum account for 8 – 16 meq/L of unmeasured, negatively charged particles.

Osmolal Gaps:

While we’re on the topic of measured and unmeasured particles, there is just one more concept to introduce: the osmolal gap (OG). Particles that are small enough and numerous enough to change the osmolality of the serum, but may or may not carry a charge, are considered osmotically active. The major osmotically active particles in serum are sodium and its associated anions, glucose, and urea (a waste product of protein metabolism). When urea is being carried in the blood, it is called “blood urea nitrogen” or BUN. As you may have guessed, there is an equation to calculate serum osmolality:

2[Na+] + [glucose]/18 + [BUN]/2.8

Sodium concentration, measured in meq/L, is multiplied by 2 in order to account for the anions (chloride, bicarb, proteins, etc.) associated with it. Glucose and BUN concentrations are measured in mg/dL, and are divided by 18 and 2.8, respectively, to account for their osmotic activity relative to their molecular weights. The normal calculated osmolality of the serum is 280 – 300 mosm/kg. Serum osmolality can also be measured, typically by means of determining freezing point depression. There are, of course, other osmotically active particles in serum that are not measured by the formula above. The difference between the measured serum osmolality and the calculated serum osmolality is called the osmolal gap (OG):

OG = serum osmmeas – osmcalc

A normal serum OG is less than 12. If an individual ingests a substance that results in increased osmotically active particles in the serum, then there will be an osmolal gap that is greater than normal.

Non-Anion Gap Metabolic Acidosis:

Non-anion gap metabolic acidosis results from a loss of bicarb. The other major anion in serum, Cl-, goes up in this condition (to maintain neutrality of charges in the serum) and thus this condition is also called hyperchloremic metabolic acidosis. Bicarb is a measured particle and thus there is no anion gap when the AG is calculated with this acidotic state. Medical conditions that can cause a non-anion gap metabolic acidosis are:

  1. Diarrhea
  2. Certain drug ingestions (e.g. acetazolamide, which interferes with HCO3formation)
  3. Renal dysfunction

Anion Gap Metabolic Acidosis:

The most complicated category of acid-base disorders is that of anion gap metabolic acidosis (AGMA). For those who like to play the part of Sherlock Holmes and solve mysteries or, more contemporarily, play the lead detective in CSI (crime scene investigator), this is the category for you. Many conditions or ingestions of toxins can result in an anion gap metabolic acidosis. In order to determine the cause of this acidotic state, we have to categorize these patients based on the patient’s history and physical exam, and on lab tests: e.g. determine if there is an osmolal gap.

Many substances and conditions can cause an anion gap metabolic acidosis. A useful, but not quite complete, mnemonic is MUDPILES. This stands for:

Methanol – turns to formic acid

Uremia – acidosis from renal failure

Diabetic ketoacidosis – develop “keto acids” in Type I diabetes mellitus

Paraldehyde – a drug rarely used, develop lactic acid

Isoniazid, Iron – excess of both result in cellular anaerobic metabolism and lactic acid formation

Lactic acid – many causes of anaerobic cellular metabolism

Ethylene glycol – metabolized to glycolic acid

Salicylates – salicylic acid and causes anaerobic cellular metabolism and formation of lactic acid

All of these substances can cause an anion gap metabolic acidosis. For a list of those that cause and do not cause an osmolal gap in the setting of this acidosis, refer to the list below.

Examples of Conditions and Substances that Cause AGMA With Normal and Elevated Osmolal Gap

Normal Osmolal Gap Elevated Osmolal Gap

1. Diabetic Ketoacidosis 1. Methanol

2. Lactate 2. Ethylene Glycol

3. Salicylates 3. Alcoholic ketoacidosis

4. Toluene

Compensatory States for AGMA:

It is not uncommon for the pH to be profoundly low in a state of an anion gap metabolic acidosis. In order to compensate for this condition, the respiratory system is triggered to breath more rapidly and more deeply in order to exchange a greater volume of air with the environment and lower the pCO2 in the alveolus. This increase in respirations ultimately leads to a decrease in pCO2 in the serum, and an increase in pH. A compensatory response will only bring the pH up to a point that it gets close to a lower normal range; compensatory excess respirations will not be such that the pH will ever become greater than 7.40 (alkalotic).

Pathophysiology and Treatment of Specific Emergency Metabolic Acidotic Conditions:

Because metabolic acidosis is the most common A/B disorder you will encounter in emergency medicine, it is worth taking a look a few specific, common and important, examples.

Methanol Poisoning: Methanol, found in many places, such as window washer fluid and camping fuel, is one of the substances that, if ingested, leads to a metabolic acidosis with both an anion gap and osmolal gap. In the form of methanol, this alcohol is an intoxicant just like ethanol (EtOH) and does not cause acidosis. If it were to stay in this form, it would, in time, be fully excreted by the kidneys and no additional harm would occur. When metabolized, however, by alcohol dehydrogenase (the same enzyme that breaks down EtOH), and then by formaldehyde dehydrogenase, methanoic acid (aka. formic acid) is produced (Figure 9), and this is a strong organic acid that causes many serious consequences (severe acidosis, retinal damage leading to blindness, cellular toxicity).

C:\Users\Steve\AppData\Local\Microsoft\Windows\INetCacheContent.Word\metanol metabolism.jpg

Figure 9

Basic chemical equation revealing the metabolism of methanol in the body (which primarily occurs in the liver)

The treatment of methanol poisoning, then, is directed at blocking its conversion to formic acid and enhancing elimination. Ethanol has been the traditional treatment of methanol poisoning, as it competes with methanol for metabolism by alcohol dehydrogenase. At a level of 100 mg/dL (which is the same as 0.100 g/dL, or 0.100%, which means that one 1000th of blood volume is ethanol), ethanol can overwhelm alcohol dehydrogenase and markedly limit the metabolism of methanol.

A more novel treatment for methanol poisoning, and one used more commonly than ethanol, is fomepizole. Fomepizole also competitively inhibits alcohol dehydrogenase thus blocking the metabolism of methanol to formaldehyde. As a result, similar to the case of using EtOH, the kidneys have time to slowly clear methanol in the urine and the liver has a manageable level of formic acid that it can metabolize before it induces harmful effects on tissues of the body and before concentrations get high enough to cause a serious state of acidosis.

To enhance elimination, and to clear toxins already in the blood, emergent hemodialysis is often used as an adjunct to fomepizole in cases of severe methanol poisoning. If these therapies are instituted early, the patient is likely to suffer no serious long term consequences. If the diagnosis, and then treatment, is delayed, patients can suffer permanent blindness, severe global cellular toxicity, profound acidosis, and even death.

Ethylene Glycol Poisoning: Ethylene glycol (EG), most notably found in antifreeze, causes much of the same problems as methanol poisoning, and it has a similar pathophysiology. It too is just a mild intoxicant when in its “parent form,” but when metabolized, like ethanol and methanol, by alcohol dehydrogenase, it forms glycoaldehyde, which in turn is metabolized by the enzyme aldehyde dehydrogenase to its highly toxic metabolite, glyoxylic acid (which in turn is metabolized to 3 more organic acids that we do not need to mention). Treatment is the same as for methanol poisoning: block the metabolism of EG by competitively inhibiting the enzyme, alcohol dehydrogenase. Once again, this can be accomplished by administering EtOH intravenously, or by giving fomepizole IV. The latter is given more commonly due to the fact it doesn’t cause the altered sensorium that giving EtOH does, it has a more predictable dose response and duration of action, and may be more effective, but clinical superiority of fomepizole has not been established.4 If ethanol is all you have available, administer it, otherwise, the current standard is most supportive of fomepizole.

Other things to consider in the treatment of both methanol and ethylene glycol poisoning are, the degree of acidosis and the duration of exposure. Early after ingestion, there may be little acidosis and no evidence of renal injury. With late presentations, you are likely to see profound acidosis and evidence of renal insufficiency, particularly with EG poisoning. You are also likely to see hypocalcemia, particularly with EG poisoning.6 So, obtaining a basic chem panel, including a Ca2+ level, a serum osmolality, and an ABG would be appropriate, and intervene as appropriate. Supplemental intravenous fluids are uniformly necessary, and normal saline infusion should be started early to prevent dehydration and enhance renal elimination of toxins. Treating with thiamine, folic acid, and pyridoxine can optimize nontoxic metabolic pathways for elimination of EG and methanol, and their metabolites.6

Diabetic Ketoacidosis: (link to Endocrine module, pathophys/tx section)

Acidosis of Renal Failure: The kidneys produce bicarb in the proximal convoluted tubule of the nephron. In renal failure, there are a lack of nephrons producing bicarb. Because the body continually produces acids, about 70 meq H+/day3, it would only take about 5 days for the body to use up more than half of it’s buffering capacity, and a state of severe acidosis would begin to ensue. Without the body producing an adequate amount of bicarb in a state of renal failure, a patient must take in exogenous bicarb in some form in order to prevent acidosis.

Acetazolamide and acidosis: Acetazolamide inhibits the production of bicarb in the proximal convoluted tubule and results in alkaline urine. The resulting metabolic acidosis has been its explanation, at least in part, for being beneficial as a treatment of high altitude sickness. Being acidotic allows the person at altitude to breathe more fully and not develop the respiratory alkalosis that would otherwise result from hypocarbia (low CO2). It’s mechanism of action in “acute mountain sickness” is actually more complex than this, but just know that this medication causes a direct non-anion gap metabolic acidosis.

Metabolic Alkalosis:

The last acid/base condition to discuss is metabolic alkalosis. This can be the result of loss of H+ from excessive vomiting or an accumulation of excess HCO3. Ingestion of a large amount of a base, e.g. sodium hydroxide (baking soda) or magnesium hydroxide (found in antacids), can result in a significant metabolic alkalosis.

Drugs such as acetazolamide block bicarb production in the proximal renal tubule and results in a bicarb diuresis. This can be used to treat metabolic alkalosis. As the kidneys attempt to compensate for a metabolic alkalosis, they excrete K+ in the distal tubules and exchange for H+ that is reabsorbed. This can result in a profound and critically dangerous state of hypokalemia.

Work-up, Diagnosis, and Management of Emergency GU Related Chief Complaints:

Dysuria female: link to Ob/Gyn module

Dysuria: male:

Dysuria scenario #1:

A 64-year-old male presents with painful urination and trouble emptying his bladder. He has felt more tired over the past 3 – 4 days and has been experiencing intermittent chills. The patient’s wife encouraged him to go to the emergency department this afternoon since she hasn’t been able to get him to get out of bed today because of his “weakness.” He is normally quite active, playing tennis at least two times per week. He has not vomited, but doesn’t have much of an appetite.

PMH: hypertension, for which he takes atenolol and losartan. He is also on a baby aspirin daily – his only other medication.

On exam, the patient’s BP is 130/80, HR 80, T 99.4°. He appears mildly diaphoretic and has a hard time sitting up without assistance.


What is your differential diagnosis for this patient’s pain?

Please write your answer then open the pop-up card by clicking here.

Pop-up card: There are several conditions to consider in patients with acute dysuria. Urinary tract infection is certainly a strong possibility, and with fever this would be pyelonephritis. Another potential etiology would be acute prostatitis: patients may have similar presentations as they do with acute cystitis.9 Diverticulitis, with inflammation near the bladder, can give bladder symptoms and even pyuria. Other intra-abdominal etiologies would be less likely without more abdominal pain or other GI symptoms. STD’s in the elderly are not uncommon and should be considered in the differential diagnosis.

What tests do you want to order to work-up this patient’s condition?

Please write your answer then open the pop-up card by clicking here.

Pop-up card: Clearly a urinalysis with urine culture would help you to make your diagnosis. Most providers would also obtain a CBC and basic chem panel, but blood cultures along with a lactic acid level would also be important to look for and manage sepsis. A CT scan of the abdomen, at this point, is not likely to give you any additional useful information, or at least isn’t necessary.

The urinalysis returns revealing pyuria with 25 WBC’s/hpf, no blood, and no bacteria are seen on micro. The peripheral WBC count is elevated at 14,000, and the chem panel is all normal. His lactic acid is normal at 0.8.

What is your diagnosis, or is there another test you want to do first?

Please write your answer then open the pop-up card by clicking here.

Pop-up card: Pyuria alone does not diagnose UTI or pyelo, you still need to evaluate for prostatitis. In this case, a careful rectal exam should be performed to examine the prostate. If a normal median fissure is felt and the prostate is non-tender, this is not likely prostatitis.

Rectal exam is performed and reveals an enlarged, boggy, and tender prostate. You make the diagnosis of acute prostatitis.

Management: This patient is not septic, but this is not a simple case of prostatitis. He is weak, febrile, having chills, and is at risk for bacteremia and sepsis. At least a short stay hospitalization is warranted for this patient while you initiate therapy. You administer Ciprofloxacin 400 mg IV in the ED.

Outcome: , After 2 days in the hospital with IV fluids and additional antibiotics, he goes home on long-term antibiotics to fully clear this infection. He does well at follow-up.

Dysuria Scenario #2:

A 22 year old male presents with a 4 day history of progressive dysuria, and slight blood tinged urine over the past 24 hours. He is going to the bathroom more often than usual and has urgency of urination as well. He has no fever or nausea/vomiting. He denies back pain but has mild feeling of “fullness” in the suprapubic region. He has not sustained any recent trauma, is otherwise healthy, and has not had a problem like this in the past.

On exam, BP 120/75, HR 78, T 98°. He appears well clinically.

What is your differential diagnosis for this patient’s pain?

Please write your answer then open the pop-up card by clicking here.

Pop-up card: This clinical presentation seems to be most consistent with acute cystitis, which, in males, would make this a complicated UTI. Other possibilities include urethritis, most commonly from an STD, but this would usually manifest with some penile discharge and would be less likely to have associated hematuria. Prostatitis would be less at this young age but still possible and should be considered.

What tests do you want to perform to work-up with patient’s disorder?

Please write your answer then open the pop-up card by clicking here.

Pop-up card: A urinalysis with urine culture would be important, but blood tests are not likely to be helpful. Imaging tests are also not indicated at this point. Testing for STD’s with a penile swab, or at least testing the urine, could be beneficial and should be performed if there are any risk factors for STD’s. Examining the prostate can also help you to rule in or rule out prostatitis.

Results: The urine returned with greater than 100 WBC’s/hpf and few bacteria. He has no penile discharge, but a swab for GC/Chlamydia was sent. His prostate exam was normal.

You diagnose acute cystitis.

Management: Your lab has found that TMP/SMX has been effective against E. coli locally, so you start the patient on a double strength tablet twice daily for 2 weeks.

Outcome: The patient, at clinic follow-up, was found to have grown > 100,000 E. coli on urine culture. He was symptomatically improved after his course of treatment and had a clear urine.

Dysuria Scenario #3:

22 year old male presents with a 2 day history of painful urination and purulent penile discharge. He has had no fever or groin/testicular pain. He has no frequency of urination or flank pain. He does admit that he has a new sexual partner, but she stated she is not having any symptoms suggestive of an STD.

The patient has no chronic medical problems and is on no medications.

On exam, vital signs are normal, his abdomen is non-tender, and he has purulent drainage expressible from the urethral meatus.

What is your differential diagnosis for this patient’s pain?

Please write your answer then open the pop-up card by clicking here.

Pop-up card: This is a classic presentation of acute urethritis, and the usual pathogen in a case like this is either N. gonorrhea or Chlamydia. This diagnosis is so likely, and the patient’s presentation is so benign, that other diagnoses really do not have to be entertained until this diagnosis is disproved.

What tests do you want to perform in this case?

Please write your answer then open the pop-up card by clicking here.

Pop-up card: There are no tests that need to be ordered in this case, as you are going to treat this patient for gonorrhea and Chlamydia despite the result of any tests. A urethral swab may be helpful for public health purposes, but this patient’s sexually partner should seek treatment for an STD as this person is also likely infected. Women commonly have little symptomatology with cervicitis related to an STD.

Treatment of acute urethritis in males is straightforward, and after a discussion with the patient you elected to give him ceftriaxone 250 mg IM and 1 gram of azithromycin P.O.

Outcome: This patient did not follow-up with his primary provider, but you did obtain a urethral swab and this did return positive for Chlamydia. The result was sent on to the state’s department of health, and the case was investigated to be certain that all sexual contacts were treated.

Dysuria Scenario #4:

A 74 year old male presents because of frank hematuria and mild dysuria. This just started in the past 12 hours, but he has had blood with urination all three times that he has passed urine over this time period. The patient denies fever, nausea, fatigue, or lightheadedness. He is not on anti-coagulants.

On exam: no fever, blood pressure 130/85, heart rate 76. He is well appearing.

What is your differential diagnosis for this patient’s pain?

Please write your answer then open the pop-up card by clicking here.

Pop-up card: Hematuria can be caused by bleeding within the kidney (from tumors, various nephropathies, infection or other inflammatory causes, or stones), from the ureter (most commonly from a partially obstructing stone), from the bladder (as a result a complication of a simple cystitis, but can also be a sign of a urologic tumor that has now eroded to the surface and caused bleeding), or from the urethra (from trauma – e.g. placing a foreign body in the ureter, or infection, rarely from a tumor). A bleeding disorder can cause bleeding from any of these locations. Also consider trauma, but this should be evident by careful history and exam.

What tests do you want to order on this patient?

Please write your answer then open the pop-up card by clicking here.

Pop-up card: A urinalysis with urine culture would be a good start. A CBC with platelets would also be helpful, to be certain he is not anemic or thrombocytopenic. Coag studies, INR and PTT, are not likely to abnormal without some other clinical indication, but ordering these may be useful. For new significant hematuria, a CT scan of the abdomen and pelvis is necessary to evaluate renal mass and calculi within the kidneys and ureters.

Results: The urine test returned revealing > 100 RBC’s/hpf, 5 WBC’s, and no bacteria on micro. The patient’s hemoglobin is at the low normal range of 13.6 g/dL, and his platelets are normal at 190,000. You did not order coag studies. A non-contrast CT scan of the abdomen and pelvis reveals no evidence of renal mass or inflammation, or calculi along the urologic pathway. It is a normal study.

What is the likely diagnosis and how will you manage this patient?

Please write your answer then open the pop-up card by clicking here.

Pop-up card: In the absence of a renal mass or infection, additional diagnostic studies need to be performed. The next step, in this age group, is to refer this patient to a urologist for a retrograde cystoscopy so bladder cancer can be investigated.

Management: This patient’s diagnosis, at this point, is simply “hematuria.” You decide to place a urinary catheter and he is found to have frank blood for urine output. You talk to the on call urologist and institute continuous bladder irrigation as he needs to be admitted to the hospital due to ongoing significant blood loss.

Outcome: The patient’s hemoglobin drops to 11.2 g/dL by morning, when he is evaluated by the urologist. He is taken to the operating room and found to have bladder cancer (specifically, transitional cell carcinoma). This is managed surgically and the patient was discharged on the first post op day.

Unable to urinate (urinary retention):

Urinary retention scenario #1:

74 year old male presents with an inability to pass his urine and a feeling of a very full bladder. He has been having trouble getting a good stream of urine for months but has not sought care for this. On exam, he is afebrile, BP 170/80, HR 92, and he is standing and pacing in the room because of severe pain.

What is your differential diagnosis for this patient’s pain?

Please write your answer then open the pop-up card by clicking here.

Pop-up card: This patient clearly has urinary retention and needs to have his bladder emptied. No additional diagnoses need to be entertained at this point before you intervene to assist him.

What are you going to do to help this patient?

Please write your answer then open the pop-up card by clicking here.

Pop-up card: I’m sure you guessed it…immediate placement of a urinary catheter.

Results: 900 mL of urine drain into a urinary bag and the patient has relief of his symptoms. You send a UA and it comes back normal (no signs of infection).

How would you like to manage this patient?

Please write your answer then open the pop-up card by clicking here.

Pop-up card: Sending the patient home with the urinary catheter in place is wise, as he is simply likely to develop recurrent urinary retention if you take it out. In addition, alpha blocker therapy has been found to be useful in patients with BPH to decrease the size of the prostate and improve urine flow. Keep in mind, though, that you have not ruled out underlying prostate cancer, and this patient needs close urologic follow-up.

Outcome: You discharge the patient from the ED with a leg bag for his urinary catheter and start him on Tamsulosin 0.4 mg daily and give him a 10-day supply and instructions to see his urologist within the next 3 days. He does well at follow-up, but does ultimately require surgical intervention to regain adequate urine flow.

Urinary retention scenario #2:

A 45 year old woman with uterine prolapse and incontinence of urine presents 1 day post op from a laparoscopic assisted vaginal hysterectomy and bladder suspension surgery, now unable to urinate. She has a full bladder but otherwise a benign abdominal exam, and she is afebrile with normal vitals.

What is your differential diagnosis for this patient’s pain?

Please write your answer then open the pop-up card by clicking here.

Pop-up card: Another straight forward case of urinary retention with just one answer…pass the urinary catheter.

Management: A UA can be sent, but no other tests are likely to be of use. The patient will need to follow-up with her surgeon to see when her urinary catheter can be removed. She is sent home with a leg bag and the urinary catheter in place. There is obviously no role for alpha blockers in this case.

Outcome: With healing of surgery and the decreased inflammation over time, the urinary catheter was able to be removed after just 2 days, and the patient did well thereafter.

Flank pain:

Flank pain scenario #1:

32 year old female presents with right flank pain radiating to the right groin area, that has been increasing for the past 3 days. She has no dysuria, but has noticed some blood in her urine, and she is not menstruating as her last period was 2 weeks ago.

Her exam reveals BP 110/65, HR 115, RR 18, T 99.4. She appears tired but she is answering questions and sitting up.

She tenderness in the region of the right costovertebral angle, and minor tenderness to the right lower quadrant and groin.

What is your differential diagnosis for this patient’s flank pain?

Please write your answer then open the pop-up card by clicking here.

Pop-up card: The differential diagnosis in this case of flank pain is very broad, and we will need to consider diagnoses outside of the GU system.10 Flank pain radiating to the RLQ is a classic presentation for ureteral obstruction from a renal stone, but appendicitis, particularly a retrocecal appendix, can cause right flank pain with RLQ pain. Pyelonephritis, pelvic inflammatory disease, and other inflammatory intraabdominal and pelvic processes can also present this way. For further discussion of the differential of flank pain, please play the video below.

Insert flank pain vid lesson

Return to flank pain scenario #1:

So, what lab tests do you want to order on this patient in order to diagnose the cause of her flank pain?

Please write your answer then open the pop-up card by clicking here.

Pop-up card: Obtaining a urine specimen from this patient would be a great place to start your work-up. Not only can you look for infection and blood, but you can also determine if she is pregnant, as that would complicate this case further. A urine specimen obtained via “straight cath” is ideal, but most women prefer not to go through that, and frankly it isn’t generally necessary. Giving the patient adequate perineal cleansing instructions and informing her of the proper technique of giving a “clean” urine specimen is usually adequate.

Other tests that are likely to be useful are blood and urine cultures. Even with a low grade fever, there is a good chance that the flank pain is from an infectious cause. Given the elevated heart rate, despite a normal blood pressure, this patient could be experiencing early sepsis, so a lactic acid level would be helpful as well to look for this possibility. Most providers will also get a complete blood count in this setting, though the value of a white blood count is debatable. Getting a basic chem panel to assess fluid and electrolyte status, and renal function would also be helpful.

In the evaluation of this patient’s lab studies, we find that her urine pregnancy test is negative, she has a positive leukocyte esterase and nitrate on the urine dip, and there are greater than 100 WBC’s and RBC’s along with moderate bacteria on the microscopic view of the urine. Her peripheral WBC count is 15,000 and a lactic acid level is normal at 1.1. Her basic chem panel is normal except for a BUN of 24 (her creatinine is 1.0).

What can we conclude from these lab tests and the patient’s clinical presentation? She is not in septic shock clinically and her lactic acid level is normal. She has evidence of dehydration with her elevated heart rate and pre-renal azotemia (BUN: creatinine ratio is > 20). The clinical presentation does not suggest that she is critically ill. What diagnosis is now at the top of your differential?

Please write your answer then open the pop-up card by clicking here.

Pop-up card: Acute pyelonephritis is the most likely diagnosis in this case, but pyuria can occur with pelvic infections such as PID and acute appendicitis. An obstructing ureteral stone can also cause much pain in flank and can complicate the clinical course of acute pyelonephritis.

So, what do you want to do from here? Are there any imaging studies that would be useful? Are there imaging studies you should avoid?

Please write your answer then open the pop-up card by clicking here.

Pop-up card: Knowing what to do is always important, but with experience, learning what isn’t necessary is important too. It is well known that new providers tend to order more tests than more experienced EM providers (whether physician or APP). The fear of missing something is real, but just ordering a test “to be sure” can introduce an unnecessary risk to the patient and even provide a false sense of security. Developing the confidence to not order tests comes with time and experience, so we won’t be able to replace that clinical piece here, but let’s walk through the thought process of what to order and what not to order in this particular case – looking through the evidence based lens of the emergency physician.

First of all, assess how sick she is. She is not in septic, and in fact she is otherwise healthy, without comorbidities such as diabetes, and appears to have a pretty benign illness. Her abdomen is benign, minimally tender, on exam and her clinical course has been 3 days. Acute appendicitis is very unlikely. If she has any risk factors for PID, a pelvic exam should be performed, cultures for GC and Chlamydia should be obtained, and you should assess for cervical motion and adenexal tenderness that would be suggestive of PID. A CT scan of the abdomen and pelvis is not likely to change your management in this case, so this should be avoided as it is an expensive test that will expose this patient to unnecessary radiation. It would be reasonable to simply treat this patient empirically for acute pyelonephritis, but an ultrasound of right kidney would be reasonable to perform if the patient has a history of renal calculi or there is clinical suspicion of this. An ultrasound of the right lower quadrant to evaluate for acute appendicitis could be reasonable if the exam is at all suggestive.

Caveat: There are no two patients that present clinically identical, so adjusting your work-up and management to fit individual needs is always important. There are multiple ways that this case can be managed, and the purpose of this exercise is give the new provider an indication of a general, evidence based and clinically reasonable approach.


How do you want to manage this patient? Since her abdominal exam is benign, her flank pain came on gradually over 3 days and is not acutely worse today, and she has no risk factors for STD’s and no pelvic pain, we will conclude that she has acute pyelonephritis. Since this doesn’t seem to be complicated by sepsis or an obstructive process, this patient can probably be managed as an outpatient if she can eat (stay hydrated) and hold oral medications down.

What treatments do you want to initiate in the ER?

Please write your answer then open the pop-up card by clicking here.

Pop-up card: This patient clearly needs hydration, and the best way to do that is intravenously with crystalloid: usually about 2 liters of normal saline. Next, she needs an antibiotic. If you are not sure if she will be admitted or not, starting with ceftriaxone, 1 to 2 grams IV, would be appropriate. Using an anti-emetic, such as metoclopramide or ondansetron, would be useful to help control nausea and allow her to prove, in the ER, that she can hold PO’s down (give her an oral challenge with juice and crackers). If she needs a small dose of an opiate to control pain, e.g. morphine 4 mg IV, that would be helpful – some patients simply prefer to use acetaminophen.

ED management: After 2L NS IV, 1 g of ceftriaxone, 5 mg IV metoclopramide, and 4 mg IV morphine, the patient is feeling much better, her heart rate is 88 bpm, BP is still normal, she is taking fluids orally and even ate some toast. You elect to send her out on ciprofloxacin 500 mg bid for 10 days. She is ambulatory without lightheaded and appears well at discharge from the ED. You gave her some metoclopramide to use at home for nausea, and she did not want any oral opiates for pain.

Outcome: The patient followed up with her primary provider in 2 days, as you directed, and her urine culture grew > 100K E. coli. Both sets of blood cultures revealed “no growth.” Her flank pain was resolved and she was eating well. She finished her course of antibiotics and reported to her primary doctor again that she was doing well.

Flank pain scenario #2:

74 year old male, presents with acute onset of right flank pain that is severe and sharp. He feels nauseated and has vomited several times. He has had no urinary symptoms, fever, or recent trauma. He denies chest pain or shortness of breath. No numbness, weakness, or shooting pains to lower extremities.

Exam: Temp 97.8, BP 150/90, HR88, he is pacing and in severe pain – cannot get comfortable. His abdomen seems benign, but he is moderately obese.

As you proceed with your work-up, be certain to have your nursing staff obtain IV access and give this gentleman something for pain: titrating hydromorphone, 0.5 mg per dose IV, would be reasonable.

What is your differential diagnosis for this patient’s flank pain?

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Pop-up card: Generating a differential diagnosis in an elderly person is commonly much more difficult than in the young because there are many more diagnoses to consider, many of which involve vascular disease. In emergency medicine, we consider the “worst first” diagnoses before we settle in on the more benign, and perhaps less common, causes. So, in this gentlemen, entertaining the possibility of AAA is important. Causes of renal colic should be considered next, including pyelonephritis, hydronephrosis (from an obstructive process), and renal infarct – a diagnostic possibility we haven’t discussed yet in this module, but a very rare cause of flank pain compared to the others mentioned. Intra-abdominal processes, such as diverticulitis, can cause flank pain, but are usually accompanied by significant abdominal tenderness. Musculoskeletal causes of flank pain should be considered next, including muscle strain and disk herniations. Finally, consider dermatologic causes, such as herpes zoster.

What tests would you order for this patient?

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Pop-up card: Point of care ultrasound would be an appropriate first step, as a normal caliber aorta would immediately rule out AAA in this at risk patient. This study can be difficult in obese patients. Next, a CT scan of the abdomen and pelvis without IV contrast could evaluate for ureteral calculi and adequately assess for intra-abdominal disorders such as diverticulitis. Routine labs are typically sent at this point as well, including UA, CBC, and Chem panel.

Results: Labs return and the UA reveals hematuria but no signs of infection. Other labs are normal. A non-contrast CT scan of the abdomen and pelvis reveals a 3 mm distal ureteral calculus at the UVJ and moderate hydronephrosis.

Management: This patient needs pain control for renal colic secondary to his obstructing ureteral stone. Since it is near the bladder and relatively small, there is a good chance that this will pass without requiring surgical intervention. You send the patient home with oxycodone for pain. Some studies have found that alpha blockers are also helpful in getting ureteral calculi to pass, so you send him home with a prescription for tamsulosin, 0.4 mg daily for 5 days.

Outcome: The patient strained all of his urine at home and passed a small calculus within 36 hours of leaving the ED. He was well at follow-up with his primary provider.

Flank pain scenario #3:

A 35 year old female presents with right flank pain that has been intermittently severe for the past 5 days. It is now continuously severe. She has associated nausea and vomiting, and this has been worse over the past day. She is feeling globally weak and fatigued and has decreased appetite. She has had dysuria but has not noticed hematuria. She denies abdominal or pelvic pain, and has not had vaginal discharge. Her last menstrual period was 3 weeks ago and she is 2 years status post tubal ligation. She denies any chronic medical problems, is on no medications, and has no known allergies.

On exam: BP 85/60, HR 125, T 102.4°. She is diaphoretic and is clearly in pain distress.

What is your differential diagnosis for this patient’s flank pain?

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Pop-up card: Even though this patient’s major concern is her flank pain, in the eyes of the emergency provider, she is critically ill and showing signs of sepsis. The differential diagnosis in this case, then, will be related to infectious causes of her sepsis. Clearly pyelonephritis with urosepsis is on the top of the list. Appendicitis, particularly a ruptured retrocecal appendix, could cause flank pain and fever. Fitz Hugh Curtis Syndrome (purulent STD, typically gonococcal, infection that spreads to the perihepatic area) can also cause this presentation, but is quite rare and should be associated with much pelvic pain. Right sided diverticulitis could cause this pain as well, but this would be rare in this age group. With the severity of the pain, one always has to consider a concomitant ureteral calculus in the setting of pyelonephritis: a urologic emergency.

What tests would you order for this patient?

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Pop-up card: With clinical evidence of sepsis, she needs to have blood cultures and a lactic acid level performed. You will also need a urine specimen for a UA and urine culture, and given her hypotension and signs of sepsis, obtaining this specimen via a straight cath will be the most efficient and accurate means to do so. A CBC and basic chem panel will also be useful.

Because this patient is critically ill and has severe flank pain, obtaining a study to evaluate for ureteral obstruction would be important. This can be accomplished via renal ultrasound or non-contrast CT of the abdomen and pelvis. Providers skilled in POCUS (Point of Care Ultrasound), can look for hydronephrosis at the bedside while other work-up and intervention procedures are performed: e.g. starting IV’s and giving fluids and pain meds.

Results: Labs return revealing UA with >100 WBC’s/hpf, few RBC’s, and few bacteria. POCUS of the right kidney reveals a dilated renal pelvis. This drives you to get a non-contrast CT scan of the abdomen and pelvis and this reveals a 6 mm proximal ureteral calculus with moderate hydronephrosis. Peripheral WBC count is 18,000, and a chem panel is normal. Lactic acid returned high at 5.2.

What treatments would you institute on this patient?

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Pop-up card: You would not have waited for lab tests to initiate some early interventions, including an IV fluid bolus of normal saline (1 -2 liters) and administration of pain medications. When the lactic acid test returned high, the first test to return, you started the patient on meropenem, 1 g IV (piperacillin/tazobactam 3.375 to 4.5 g IV would be another good choice). When the renal ultrasound reveals hydronephrosis, you contact the on-call urologist and arrange for transfer of care to this provider. Before bringing this patient to the OR, the urologist requests a non-contrast CT scan of the abdomen and pelvis and you inform him that this is already being carried out. You give additional IV fluids, up to 30mL/kg, and the patient is sent on to the urologist.

Outcome: The patient was met by the urologist in the OR. Via retrograde catheter placement, the stone was pushed up into the renal pelvis and a double J stent was placed in the ureter to keep it open. Purulent urine drained. Within 24 hours the patient’s fever defervesced, the blood pressure normalized, and the patient began to feel much better.

Flank pain scenario #4:

72 year old dentist was riding a tractor on his hobby farm much of the previous day and now presents with a nagging low back ache and right flank pain. He has no burning or frequency of urination and no fever. He has no numbness or weakness to the legs. He has no nausea or other bowel symptoms.

Exam: T 98, BP 110/60, HR 94, he is standing and clearly has severe pain. He doesn’t seem to have much back tenderness. His lungs are clear. When he lays down, you find his abdomen to be non-tender.

What is your differential diagnosis for this patient’s flank pain?

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Pop-up card: The differential diagnosis in this case include the usual suspects of acute back and flank pain: urologic causes – including renal stone disease, vascular causes – including AAA, zoster, and mechanical back pain. With his history of being on the tractor, he is telling you that he thinks this is just his back that is giving him trouble. Beware, though, of the seemingly benign presentation in the elderly patient.

What tests would you order for this patient?

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Pop-up card: A urine test would be useful, but you decide to do a POCUS of the abdomen to look for AAA since it is easy to perform and readily available.

Results: A bedside ultrasound reveals a 10 cm AAA but no free fluid in the abdomen. Note that you cannot typically determine AAA with rupture to the retroperitoneum with ultrasound, but that has to be assumed in this case. Two large bore IV lines are started and the patient is sent for immediate contrast CT scan of the abdomen and pelvis. As this patient with stable vitals moves to the CT scanner, you talk to the on call vascular surgeon and arrange transfer of care to this provider.

Outcome: The CT scan reveals retroperitoneal rupture of a 10 cm AAA. The patient is flown by medical helicopter to a tertiary institution with the on call vascular surgeon you talked to. The patient went to the OR immediately and upon opening the abdomen, the AAA burst anteriorly spraying blood throughout the abdomen. The patient lost his pulse transiently, but was resuscitated with IV fluids, O negative blood, and a dose of epi (1 mg). Bleeding was controlled, the AAA was repaired, and the patient was sent to the ICU where he remained in critical condition for 3 days before he could be extubated. Long term he did quite well.

Atraumatic scrotal pain:

Scrotal pain scenario #1:

18 year old male presents with acute severe right testicular pain. He had a mild ache in the testicle when he awoke 4 hours ago, but it has suddenly become severe over the past hour. He denies nausea or vomiting, abdominal pain or flank pain. He has not noticed blood in his urine and has not experienced hematuria. He admits to being sexually active but denies penile discharge or history of an STD. He has not experienced fever or chills.

On exam, T 98.2, BP 130/85, HR 110.

The patient has a benign abdomen, no obvious sign of an inguinal hernia, and a right testicle that is drawn up, suspended in a normal position, and tender over the superior pole. He does not seem to have tenderness over the lower testicle or the spermatic cord. There is no evidence of scrotal redness or edema.

What is your differential diagnosis for this patient’s scrotal pain?

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Pop-up card: For acute atraumatic scrotal pain, the list of common potential diagnoses is fairly limited. These include:

  • Testicular Torsion
  • Torsed testicular appendage
  • Creamasteric strain
  • Sexually Transmitted Infection, e.g. Gonorrhea or Chlamydia are common pathogens in this case
  • Epididymitis
  • Referred pain, e.g. renal colic secondary to an obstructing stone

What tests or intervention would you perform for this patient?

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Pop-up card: Since the patient’s testicle is lying in a relatively normal position and the tenderness he has is over the superior pole, this looks, clinically, most like a torsed testicular or epidydimal appendage. It would be unwise to attempt a reduction maneuver aimed to correct testicular torsion, as this would potentially induce torsion. An emergent ultrasound, though, does need to be performed in order to confirm a benign etiology of the patient’s pain, and rule out testicular torsion. Give pain control, most commonly in the form of an intravenous opiate, and get this study performed ASAP.

Discussion: As stated in the pathophysiology section of this module, testicular appendageal torsion is the most common cause of acute scrotal pain in pediatrics and one of the leading causes of pain in all age groups.23,24 There is generally less nausea and vomiting with a torsed testicular appendage than with testicular torsion. The pain can be mild at first or acutely severe.

Outcome: The patient’s ultrasound confirms torsion of the epidydimal appendix and you have controlled the pain with titrated doses of morphine. You have the patient use ibuprofen and oxycodone for pain at home. He follows up with his family doctor in 2 days and his pain is essentially resolved.

Scrotal pain scenario #2:

A 21 year old male presents with left scrotal pain that has been increasing for the past 4 days. He has mild pain with urination and some extension of pain into the left groin. He denies penile discharge, and the pain is a 7 out of 10 in severity. He denies fever, vomiting, diarrhea, or any recent trauma. He is sexually active.

Exam: T 99.2, BP 120/78, HR 98, Appears well – non-toxic, but grimaces at times with certain movements

Genital exam reveals an uncircumcised male, no penile discharge, normal exam on right hemiscrotum but on left, he is very tender over the lower testicular region and along the epididymis and spermatic cord. The testicle has a fairly normal vertical orientation. No significant inguinal adenopathy.

What is your differential diagnosis for this patient’s scrotal pain?

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Pop-up card: The differential diagnose remains essentially the same as in the previous cases, though we can consider shuffling the order here. Since his pain has been indolent in onset, isn’t severe, and the testicle is in a relatively normal orientation, the primary diagnosis in the differential is not testicular torsion. Being uncircumcised, and perhaps having a very low-grade fever, this would put him at risk for acute epididymitis, and that would be at the top of our differential in this case. This can be caused by an extension of bacterial urethritis, so an STD is still part of the differential. This could be a testicular appendageal torsion process as well.

What tests or intervention would you perform for this patient?

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Pop-up card: This patient, like all of the other patients with scrotal pain, first need pain control. In this case, this patient needs a scrotal ultrasound to look for evidence of epididymitis and rule-out other causes. A urinalysis would be helpful and a test for STD’s (usually via a urethral swab to check for gonorrhea and chlamydia) would also be wise to check.

Results: The patient’s urinalysis reveals few WBC’s on micro and no bacteria. The scrotal ultrasound reveals swelling of the epididymis, consistent with epididymitis.

Outcome: The patient has evidence of epididymitis, caused by some kind of reflux from the urethra or migration of infection from this region. Given the patient’s age, the most likely diagnosis is an STD, so you decide to treat the patient with ceftriaxone 250 mg IM and Doxycycline 100 mg PO bid for 10 days. You give him ten oxycodone (5 mg)/acetaminophen tablets via Rx to use sparingly for pain, when ibuprofen doesn’t work. The patient had follow-up with his primary provider after the antibiotics were completed and his symptoms had resolved. He was informed that his GC test was negative but chlamydia was positive, therefore his sexual partner(s) needs to be treated as well.

Scrotal pain scenario #3:

14 year old male presents with sudden severe right testicular pain, starting less than 1 hour prior to his presentation to the ER. The pain extends to the right groin region and he has nausea but no vomiting. There has been no recent trauma. He denies fever or other illness.

On exam, T 98.2, BP 135/85, HR 115. He is lying in bed in the fetal position and is clearly in severe pain.

His abdomen seems to be benign, but there is some tenderness to the right inguinal region, but no bulge or mass present. You stand him up and notice that the right testicle seems to be lying in a rather horizontal position, it is drawn up slightly higher than the left testicle, and he does not seem to have a cremasteric reflex (stroking the inside of the right thigh does not cause a drawing up of the testicle on the right).

What is your differential diagnosis for this patient’s scrotal pain?

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Pop-up card: This presentation strongly suggests testicular torsion, and time is of the essence. There are certainly other possibilities of scrotal pain to be entertained in your differential diagnosis, but because this is such a classic presentation, this is your working diagnosis at this point.

What tests or intervention would you perform for this patient?

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Pop-up card: This patient needs an IV line placed and some immediate pain control. You discuss your findings with the patient and his parents recommend an attempt empiric manual detorsion of the right testis. You defer other testing at this time.

Results: You give the patient IV fentanyl titrated for pain and ask him to bear with you as you rotate the testicle (in an “open book” fashion, so counter-clockwise for the left testicle). The patient has improvement of pain after just 180 degrees of turning but pain does persist. After another 180 degrees of turning (one full “flip” of the testicle) pain is resolved and you stop.

Outcome: You call the urologist and let him know that you just empirically detorsed a testicle based on clinical grounds alone and that you’d like him to explore this child in the OR. He agrees and comes in to evaluate this patient. He is brought to the operating room, detorsion is completed, and an orchipexy is performed. The patient has a good outcome

Scrotal pain scenario #4:

A 23 year old male presents to the ED on a winter evening with a progressive and persistent right scrotal pain that has been going on for the past 8 hours. He has tried ibuprofen, but the pain persists and is in fact getting worse. It aches at rest and is severe when the scrotum is moved or manipulated. There has been no recent trauma, no penile discharge, no dysuria, and no abdominal pain. He has some pain extending to the right groin. He is sexually active.

Exam: T 98.0, BP 135/85, HR 105, he is calm and grimaces with certain movements.

Genital exam reveals no tenderness over the testicle, some mild sensitivity over the epididymis inferiorly, and much tenderness over the testicular cord and into the inguinal region. There is no apparent bulging mass from the groin to suggest hernia. He is circumcised and there is no apparent penile discharge or any penile lesions.

What is your differential diagnosis for this patient’s scrotal pain?

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Pop-up card: This patient has an indolent onset of pain, and it isn’t acutely severe and not clinically suspicious for testicular torsion. Epididymitis is a strong possibility, as is a related STD. There is no fever and no sign of other infection. Inguinal hernia is still a possibility, and cremasteric muscle strain is in the differential.

What tests or intervention would you perform for this patient?

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Pop-up card: A scrotal ultrasound to rule out torsion is still important in this case, and it will also help to identify the presence of appendageal torsion if this is present. A urinalysis would also be useful and a test for gonorrhea and chlamydia would also be indicated.

Results: The patient’s scrotal ultrasound returns negative for torsion and there is no sign of epididymal swelling/inflammation, and no sign of appendageal torsion. The urine returns with no pyuria or bacteria on micro. The patient has no history of STD’s and denies likelihood of this.

Outcome: You will defer treatment for potential STD’s and treat the patient simply for pain. You refer him to follow-up with his primary provider, who can then make a referral to a urologist if needed. The patient’s pain goes away within 1 to 2 days, and his GC and Chlamydia tests return negative. This patient likely had a simple cremasteric strain. When following up with his primary doctor, it is discovered that this patient runs outside in cold weather in boxer shorts. It is recommended that he use a supporter when running.

Acute Renal Failure (ARF):

ARF scenario #1:

A 74 year old female presents with a several day history of a general feeling of fatigue and achiness, along with nausea, vomiting, and decreased appetite. She has mild diarrhea. She has chronic low back pain, for which she takes ibuprofen over the counter, and this pain has been worse recently. She has not vomited any blood.

On exam, T 98, BP 110/70, HR 115, she is non-toxic appearing but appears fatigued and her mouth is dry.

You check a basic chem panel and this returns: Na+ 130, K+ 4.5, Cl 98, CO2 20, BUN 68 creat 3.2, glu 88.

You look in her EMR and find a creatinine level from 4 months earlier that was normal, at 1.0.

What is your differential diagnosis for the cause of this patient’s renal insufficiency?

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Pop-up card: This patient is clinically dehydrated, related to her vomiting and poor PO intake. She has evidence of pre-renal azotemia and new renal insufficiency with an elevated creatinine. Dehydration alone can cause renal insufficiency, particularly if prolonged, but the fact that she is taking a NSAID is also likely contributing to her renal failure. Urine infection also needs to be considered, as pyelonephritis could also be a contributing factor.

What tests or intervention would you perform for this patient?

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Pop-up card: Obtaining a urinalysis would be helpful. Initiate IV fluids immediately, starting with a liter of normal saline, and monitor urine output.

Outcome: The patient was admitted to the hospital because of significant dehydration and inability to adequately take PO’s. Her renal function gradually improved after 48 hours in the hospital. She was taken off of all NSAIDS and her creatinine was improved, at 2.1, but not back to normal at hospital discharge.

ARF scenario #2:

A 34 year old male is brought in by his sister after she found him at his home appearing to be ill. She states that he has a history of substance abuse and was drinking with friends the evening of the previous day. He also admits to cocaine use and states that things got out of hand as he used more cocaine than he ever had before. He also had a lot of alcohol and hasn’t had much for fluids today as he has a decreased appetite. He has not been vomiting. He has not noticed blood in his urine.

Exam: T: 98, BP 110/75, HR 128, he is diaphoretic, tremulous, and has “tongue wagging” when he opens his mouth.

You check a basic chem panel and this returns: Na+ 134, K+ 3.0, Cl 95, CO2 16, BUN 28 creat 3.4, glu 88.

You look in her EMR and find a creatinine level from 6 months earlier that was normal, at 1.0.

What is your differential diagnosis for the cause of this patient’s renal insufficiency?

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Pop-up card: This patient appears to be in alcohol withdrawal, but that doesn’t normally cause acute renal failure like this. With his cocaine use, you must consider rhabdomyolysis as a cause of ARF. Unrecognized trauma is a possibility, as this patient may not recall trauma if he was altered the night prior, but findings would generally be present clinically. An acute obstructive process is possible, but without being occluded bilaterally, this kind of rise wouldn’t occur. Since he is urinating, he isn’t completely obstructed.

What tests or intervention would you perform for this patient?

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Pop-up card: You order a CPK on this patient to evaluate for rhabdomyolysis. You also initiate IV fluids, 2L NS, and begin titrating benzodiazepines, lorazepam 1 mg every 15 to 30 minutes, to get his shakes controlled within the hour.

Results: The patient’s CPK returns at 110,000, and you diagnose him with acute rhabdomyolysis and associated ARF. You give the patient an amp of bicarb IV, and change his IV fluids to D5W with 2 amps of bicarb and run this at 1000 mL/hour over the next 2 hours until he gets admitted to the hospitalist service.

Outcome: This patient had his alcohol withdrawal managed well and slowly regained a normal appetite. His creatinine came down to 1.6 by the 3rd hospital day. He agreed to go to an inpatient drug treatment facility arranged by his family, to where he was discharged the following day.

Dialysis patient scenarios:

Dialysis patient scenario #1:

A 52 year old male, who has history of end stage renal disease (ESRD) secondary to longstanding hypertension, presents with shortness of breath. He missed his hemodialysis run yesterday, and now presents on a Tuesday evening not having dialyzed since Friday. He still produces a small amount of urine but was at relatives for the holiday and didn’t keep to his low sodium diet, as he had ham for supper 4 hours earlier. He has not had a fever or cough.

Exam: T 97, BP 195/115, HR 108, pulse ox 88% on room air. He is very dyspneic and tachypneic, and clearly struggling to breathe. He has crackles in the lower lung fields bilaterally and no obvious heart murmur. He has bilateral 2+ lower extremity edema and family states this is common for him.

What is your differential diagnosis for this patient’s shortness of breath?

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Pop-up card: This patient is clearly in CHF clinically, and it is probably related to simply to fluid overload, both from missing a dialysis run and from excessive Na+ intake. This episode of CHF code be secondary to an acute MI as well or there may be myocardial ischemia as a result of hypoxia related to CHF.

What tests or interventions would you perform for this patient?

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Pop-up card: You need to act quickly to keep this patient from decompensating to acute cardiovascular collapse (cardiac arrest). Since he is able to talk and give some history, you place him on BiPAP to assist his respirations. This does seem to help him as his oxygen saturations come up to 94% on the pulse oximeter. You order a nitroglycerine drip to reduce his afterload (systemic diastolic blood pressure specifically) and 80 mg of furosemide in an attempt to diurese some of the fluid off through his marginally functional nephrons.

You next turn your attention to diagnostic tests. A 12 lead ECG is obtained and a basic chem panel. A troponin level is also drawn in order to investigate for an acute MI. A portable chest x-ray is also obtained.


The 12 lead ECG returns revealing this:

C:\Users\Steve\AppData\Local\Microsoft\Windows\INetCache\Content.Word\hyperkalemia case.jpg

You find an old ECG in his records, and it looks like this:

C:\Users\Steve\AppData\Local\Microsoft\Windows\INetCache\Content.Word\hyperK case - baseline ECG.JPG

There is clearly widening of the QRS complex compared to baseline and in particular, the S-wave is widened. This could suggest myocardial ischemia, but it is more likely that this patient is hyperkalemic.

A point of care basic chem panel is obtained and yields the following results: Na+ 142, K+ 7.2, Cl- 110, bicarb 12, BUN 92, Creat 6.8, glu 320. The troponin returns slightly elevated at 1.6.

His chest x-ray reveals this:

C:\Users\Steve\AppData\Local\Microsoft\Windows\INetCache\Content.Word\CHF - HIPPA compliant.jpg

Now what additional tests or interventions would you perform for this patient?

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Pop-up card: This patient has severe hyperkalemia and is showing ECG changes suggestive of cardiac toxicity related to the elevated K+ level. He is also noted to be in CHF on CXR, as predicted clinically. This patient needs an emergent dialysis run, but ahead of that, you need to temporize his situation by treating his hyperkalemia.

Results: You give the patient 10 units of IV regular insulin to treat his hyperkalemia. Because his blood sugar is already elevated, you do not need to give an amp of D50, but you do need to follow his blood sugars closely. You also start him on albuterol, 10 mg by continuous nebulization through his BiPAP device. You could give an amp of bicarb as well, but with his CHF you want to wait and see how he does with this treatment. As you are obtaining a repeat ECG after the above treatments, the nephrologist calls you back and agrees that this patient needs to dialyze emergently. You arrange to have the patient transferred to the ICU. You inform the nephrologist that the ECG is beginning to look better as you examine this second ECG:

C:\Users\Steve\AppData\Local\Microsoft\Windows\INetCache\Content.Word\hyperK case - partially tx'd.jpg

Outcome: This patient’s repeat ECG reveals narrowing of the QRS and is approaching the appearance of his baseline ECG. His breathing is improved as well and he is oxygenating better. He goes to the ICU and dialyzes and is feeling much better, back to baseline, by the following morning. He understands better the need to follow his restricted fluid and sodium diet and the need to make it to all of his dialysis runs. Incidentally, his troponin was elevated, but it is always a little elevated because of his renal failure. It is likely, though, that he did suffer at least a mild myocardial injury from this event.

Dialysis patient scenario #2:

52 year old female, with history of ESRD secondary to type II diabetes mellitus and hypertension, presents with progressive redness and swelling to the right lower extremity after scratching it on the side of her wheelchair 3 days ago. She has now developed fever and is feeling weak and lightheaded. She has not been able to get out of bed today because of fatigue and global weakness and is not eating.

Exam: T 100.6, BP 78/50, HR 122, pulse ox 96%. She appears fatigued, but can open her eyes and answer questions. Her mouth is dry. Her right leg reveals deep erythema and induration below the knee with good capillary refill to the toes, but pedal pulses are not palpable.

What is your differential diagnosis for this patient’s condition?

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Pop-up card: Dialysis patients are prone to infections, and the source couldn’t be more obvious. The specific bacterial organism, though, of a tissue infection is not certain. In addition, this patient is showing some clear signs of sepsis.

Discussion: Dialysis patients are arguably among the sickest population of patients in all of medicine. Even a low grade fever, or an average normal temperature, can be a sign of a severe infection. Remember the signs of shock from the CV chapter. This patient is in a compensatory phase of septic shock. You want to intervene before she goes into terminal shock.

What tests or interventions would you perform for this patient?

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Pop-up card: IV access is a must. In hemodialysis patients, you have ready emergent access if needed: either a central line dialysis catheter or a surgically AV fistula shunt. These are only to be used, though, in dire cases: e.g. full cardiac arrest or a patient in shock and no other potential access. This patient needs blood cultures X2 sent to the lab and a lactic acid level. A CBC and basic chem panel are also necessary. If the patient produces urine that would be helpful as well, but do not let the rest of the work-up and management get held up by waiting for this. After blood cultures are drawn, immediately give appropriate antibiotics. Despite being a dialysis patient, this patient will also require volume expansion with a bolus of normal saline IV, but do this carefully as getting the fluid back will be difficult.

Results: Nursing staff was able to get peripheral IV access and obtain blood for lab tests without using the arm with the AV dialysis fistula. This patient’s WBC count came back at 18,000, hgb is near baseline at 10.8, and platelets are normal. The basic chem panel reveals Na+ 138, K+ 4.4, Cl- 104, CO2 17, BUN 38, Creat 4.2, glu 180. Lactic acid is elevated at 3.2.

Outcome: The patient received meropenem, 1 g IV, and was loaded with vancomycin as well. She was given 1500 mL of NS and her BP came up to 100/76. She was admitted to step down ICU bed (a progressive unit bed) and monitored closely. Her lactic acid level improved over the first 24 hours, and she was able to be switched to oral antibiotics on the 3rd hospital day. She was discharged home uneventfully.

Dialysis patient scenario #3: (abd pain in PD pt – bacterial peritonitiis)

A 45 year old female with history of ESRD, secondary to longstanding Type I DM, is on peritoneal dialysis and presents with a 3 day history of progressive abdominal pain. Fever has developed over the past 24 hours. She has nausea and decreased appetite. The pain is mostly on her right side, though there is radiation of pain into her back. She denies headache, neck pain, cough, chest pain, or rash.

On exam: T 99.0, BP110/80, HR 108. She is non-toxic appearing but very tender diffusely in her abdomen, particularly in the right mid abdomen. She does tense her abdomen on palpation. The site of her peritoneal catheter looks normal, without redness or swelling. She otherwise has a benign exam.

What is your differential diagnosis for this patient’s condition?

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Pop-up card: This scenario may be pointing right to bacterial peritonitis related to a dialysis catheter related infection, but do not be too quick to make this diagnosis before you rule out other causes that may be potentially surgical: e.g. appendicitis, cholecystitis or ascending cholangitis, diverticulitis with abscess or bowel rupture, or even renal stone disease with pyelonephritis.

What tests or interventions would you perform for this patient?

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Pop-up card: IV access is important. Even though the patient has a seemingly low grade or absent fever, in dialysis patients, that likely have a normal body temperature that is low at about 96° or 97°F (35.5° – 36.1°C), a temperature of 99.2°F (37.3) can be significant as a sign of infection. A CBC and 2 sets of blood cultures should be obtained, as well as a basic chem panel and a lactic acid level. Obtaining a urine specimen for UA and UC would be helpful, if this patient still produces urine. An upright chest x-ray would also be helpful to rule out pneumonia (a lower lobe pneumonia can cause abdominal pain). This patient also needs to have a sample of her peritoneal fluid sent for analysis: cell counts, gram stain, and cultures. With a dialysis catheter in place, this is a very simple sample to obtain.

Results: The patient’s chest x-ray returns normal. CBC reveals a WBC count of 12,000, hgb 10.4 and at baseline, and normal platelets. The basic chem panel reveals no significant abnormality: creatinine is elevated at baseline. The lactic acid level is mildly elevated at 2.1. The peritoneal fluid reveals a large number of WBC’s and few gram negative rods for bacteria. You elect to start the patient on piperacillin/tazobactam, 4.5 grams IV, and arrange for admission to the hospitalist service.

Are there other tests or interventions you would like to perform before this patient is admitted?

Please write your answer then open the pop-up card by clicking here.

Pop-up card: This patient’s diagnosis is peritonitis, but a source of infection is still not confirmed. A non-contrast CT of the abdomen and pelvis should be able to adequately evaluate for possible appendicitis, diverticulitis, and even cholecystitis and pyelonephritis.

Outcome: The CT scan does not reveal any acute pathology so it is assumed that this is a PD catheter line infection. The patient is maintained on IV antibiotics in the hospital and on the 3rd hospital day the PD catheter was changed. Her peritoneal fluid culture grew many E. coli. The patient continued to do well clinically and was discharged on day 4. She did well in follow-up.

Acid/Base Scenarios: Based on the lab values below, indicate the acid/base disorder. In the case of metabolic acidosis, indicate if there is and anion gap and/or respiratory compensation. For respiratory disorders, indicate if the condition is acute or chronic.

Acid/Base Scenario #1:

A 27 year old male recently returned from a trip to central America and has had diarrhea for the past 6 days. He has not had hematochezia (blood in stool), but has been experiencing some mild abdominal cramping, associated with nausea and decreased appetite. His wife brings him to the ER this evening because he is feeling lightheaded and fatigued to the point that he can hardly get to the bathroom without holding on to her. Based on the lab values obtained below, determine the acid/base disorder.

132 110 42 90 7.30/30/95/14

3.4 14 1.0

Serum Osmmeas = 284


What kind of acid/base disorder is this?

Please write your answer then open the pop-up card by clicking here.

Pop-up card: First of all, this patient did not need to have an ABG performed as part of his work-up, but for the purposes of our discussion, we will include the values here so you can make an accurate assessment of the situation. As a matter of fact, an ABG is rarely needed to determine acid/base disorders. When needed, a venous pH will suffice. An ABG is required, though, to determine the pCO2. This may be required if you need to determine if the patient is hypercapneic or is not adequately compensating for a metabolic acidosis.

Now, to this condition. To determine a particular acid/base disorder, first look at the pH. In this case the pH is mildly low at 7.3, so this is a state of acidosis. Next, look at the pCO2. In this case it also low, so there is respiratory compensation for what must be, then, a metabolic acidosis. When there is a metabolic acidosis, you have to determine if there is an abnormal anion gap. In this case the anion gap is only 8, and that is normal. So, this acid/base disorder is a non-anion gap metabolic acidosis.

What is the underlying pathophysiology of this disorder?

Please write your answer then open the pop-up card by clicking here.

Pop-up card: Why did this patient develop a metabolic acidosis? Is this a case of abnormal acid production so bicarb is being consumed? Is it a matter of renal dysfunction so the kidneys aren’t producing bicarb or is wasting it in the urine, or is it a matter of bicarb loss by some mechanism other than the kidneys? This patient has severe diarrhea and stool contains a lot of bicarb, so this is a metabolic acidosis due, primarily, to bicarb loss. There is almost never a pure disorder when it comes to medical conditions, so there is likely a small component of lactic acid production due to dehydration and some degree of decreased tissue perfusion, but checking a lactic acid level in this case is unnecessary.

How would you propose to treat this disorder?

Please write your answer then open the pop-up card by clicking here.

Pop-up card: The treatment of dehydration is crystalloid fluids. The most common fluid used in emergency medicine is normal saline, but lactated ringers would be a good choice as well (particularly if more than 3 liters of fluid will be needed in a short period of time). For a mild case of acidosis like this, giving bicarb is not necessary. What is important is decreasing the loss of bicarb by treating the diarrhea and decreasing bowel motility. In this case, this is probably Traveler’s diarrhea: for diagnosis and treatment of this condition, see the GI module. Once the patient is hydrated and the diarrhea resolves, the kidneys will create the correct amount of bicarb in order to get the patient back to a normal pH.

Acid/Base Scenario #2:

A 19 year old female presents to the ER with a complaint of shortness of breath after being taken into custody for “minor consumption.” She is clearly distressed and anxious over her predicament. She is sobbing and can barely put 2 words together because of her rapid breathing.

You obtain an ABG and basic chem panel and get the following results:


140 105 14 90

4.0 25 1.0

What is this acid/base disorder?

Please write your answer then open the pop-up card by clicking here.

Pop-up card: The ABG indicates that the pH is high, so this is an alkalosis. The pCO2 is low, so this explains the alkalosis. This disorder then is a respiratory alkalosis. If we look next at the bicarb, we see that this is normal so the kidneys have not made an attempt to compensate for this disorder yet. This is, therefore, an acute respiratory alkalosis: i.e. the bicarb level hasn’t dropped.

What is the underlying pathophysiology of this disorder?

Please write your answer then open the pop-up card by clicking here.

Pop-up card: The pathophysiology of this disorder is this patient’s anxiety over her incarceration: she is hyperventilating. Her ABG reveals that she is not actually hypoxic (low on oxygen).

How would you propose to treat this disorder?

Please write your answer then open the pop-up card by clicking here.

Pop-up card: Treatment is directed at managing the patient’s anxiety: students can web search this. Consider breathing in a plastic bag or using an anxiolytic such as diazepam. Consider discussing carpal pedal spasms that commonly accompany hyperventilation.

Acid/Base Scenario #3:

A 46 year old male suffers from chronic alcohol abuse. He presents to the ER appearing ill and actively vomiting. He’s been trying to stop drinking alcohol on his own, but every time he does he goes through withdrawal symptoms of shakes, nausea, heart racing, and fatigue. When these symptoms start he tries drinking again to avoid the unpleasant feelings. When he began drinking again yesterday, after a 3 day period of sobriety, his nausea and vomiting got even worse, to the point he is even throwing up blood. He hasn’t been able to eat for 3 days. This patient has been told by his primary doctor that he has cirrhosis, which means that his liver is severely damaged from years of alcohol use. The liver normally has glycogen stores for the body to use when it needs energy from glucose, but with advanced cirrhosis the liver does not have the ability to store glycogen effectively. When the cells cannot use glucose for energy, the body breaks down fats and proteins and metabolizes the fatty acids and amino acids that these are composed of for energy. In the process of metabolizing fatty acids and amino acids, the body produces ketoacids as a waste product.

You obtain an ABG and a basic chem panel and receive the following results:


130 95 42 54

2.9 15 1.0

Measured serum osmolality is 303 and the EtOH level is 0.134

What kind of acid/base disorder is this?

Please write your answer then open the pop-up card by clicking here.

Pop-up card: This is an acidosis, since the pH is less than 7.40. The pCO2 is low, so that doesn’t explain the acidosis, in fact it is respiratory compensation for a metabolic acidosis. The osmolal gap is elevated since the OG is 30. The AG is 20, so this is an AGMA with respiratory compensation and an associated osmolal gap.

Calculated serum osm is 273 so the osm gap is 30.

What is the underlying pathophysiology of this disorder?

Please write your answer then open the pop-up card by clicking here.

Pop-up card: This AGMA is the result of ketoacids (also called, “ketone bodies) that develop from the breakdown of fatty acids, as the body breaks down fat in the body since it doesn’t have an adequate store of glucose in the body as a source of energy. The osmolal gap is a result of the ethanol. Alcoholics that go into AKA typically do not present terribly intoxicated since they have been vomiting and commonly have abdominal pain, which makes it difficult to take very much alcohol in.

Further information about ketones: the typical ketoacids generated in diabetic ketoacidosis (DKA) and alcoholic ketoacidosis (AKA) are acetoacetic acid, acetone, and beta hydroxybutyrate. Acetoacetic acid is a precursor of both acetone and beta hydroxybutyrate, and these latter products are generated in different proportions depending on the disorder. Unlike in DKA, where the major ketones are acetoacetic acid and acetone, in AKA the major ketone is beta hydroxybutyrate. The usual hospital lab tests used to test for “ketones” do not test for beta hydroxybutyrate. It may appear initially that there are very few “ketone bodies” found in a patient with AKA, and after treatment, it is common to see measured ketone levels actually go up (as beta hydroxybutyrate is converted back to acetoacetic acid before it is further metabolized), but that is because we are not measuring the predominant ketoacid of this disorder: beta hydroxybutyrate.

How would you propose to treat this disorder?

Please write your answer then open the pop-up card by clicking here.

Pop-up card: Treatment of AKA: The treatment of AKA is directed at volume replacement, since the patient is undoubtedly dehydrated, and glucose infusion (as a substrate for cellular energy). Electrolyte imbalances are common and these need to be monitored and managed as well. Because of malnutrition, vitamin supplementation is also of critical importance. These patients also commonly experience serious alcohol withdrawal so management of that is of high importance as well, as patients can actually die of this complication.

Acid/Base Scenario #4:

A 60 year old female with 80 pack years of smoking (has smoked 2 packs of cigarettes per day for 40 years) is admitted to the hospital for severe difficulty in breathing and hypoxia. As the hospitalist caring for her you review her labs tests and find:

ABG: 7.28/75/50/38

140 98 14 90

4.0 38 1.0

Osmmeas = 296

What kind of acid/base disorder is this?

Please write your answer then open the pop-up card by clicking here.

Pop-up card: The pH is low so this is an acidosis. The pCO2 is high and this explains the acidosis, so this is a respiratory acidosis. The bicarb is high, reflecting the body’s effort to compensate, via renal production/reabsorption of bicarb, for this acidosis. Renal compensation takes significant time to occur. This is, therefore, a (partially) compensated chronic respiratory acidosis.

What is the underlying pathophysiology of this disorder?

Please write your answer then open the pop-up card by clicking here.

Pop-up card: The etiology of this disorder is likely due largely to the lung damage that has resulted from years of cigarette smoking. This is likely a patient with COPD that is experiencing an acute exacerbation of her disease.

How would you propose to treat this disorder?

Please write your answer then open the pop-up card by clicking here.

Pop-up card: There is no real good treatment for COPD. Chronic Obstructive Pulmonary Disease, by definition, is a “chronic” fixed disease that cannot be reversed. The damage to small airways and the “blebs” that occur in the lungs cannot be helped. There is also, though, typically some inflammation of the airways that also contributes to the obstruction of the airways. When there is inflammation of the airways, there may also be some bronchospasm, so bronchodilators may also work to reverse a component of this disease.

So, the treatment of a COPD exacerbation consists of a trial of bronchodilator that may give some initial benefit followed by steroids that will help to reduce airway inflammation (swelling) and open the airways. Antibiotics are commonly used as well since these patients are at high risk for bacterial infections in the airways and pus produced by these bacteria can also narrow airways. Antibiotics can also treat pneumonia – that is infection that gets down to the level of the alveoli (which also impairs air exchange).

Acid/Base Scenario #5:

An 80 year old male is admitted to the ICU for a severe urinary tract infection that has gone to the kidney and into the bloodstream. As the intensivist you review his labs and find the following:

ABG: 7.27/24/95/14

Chem: 140 105 28 90

4.0 14 2.5

Osmmeas= 303

What kind of acid/base disorder is this?

Please write your answer then open the pop-up card by clicking here.

Pop-up card: The pH is low so this is an acidosis. The pCO2 is low, so that does not explain the acidosis, so this is an indication of respiratory compensation for a metabolic acidosis. The Bicarb is low, as you would expect with metabolic acidosis. Next, look at the anion gap. AG = 140 – 106 -14 = 20, which is high. We then look at the osmolal gap. Osmcalc = 2(140) + 28/2.8 + 90/18 = 295, so the OG = 303– 295 = 8. This condition, therefore, is an AGMA with respiratory compensation, and no osmolal gap.

What is the underlying pathophysiology of this disorder?

Please write your answer then open the pop-up card by clicking here.

Pop-up card: The underlying cause of this disorder, or pathophysiologic process resulting in this disorder, brings us back to the CV chapter and our discussion of shock. In a state of shock there is decreased tissue perfusion, decreased delivery of oxygen to the cell, and the cell has to turn to anaerobic production of ATP and this results in the production of lactic acid. So, this shock patient is experiencing a lactic acidosis, which in turn is the cause of the AGMA. Incidentally, shock is caused by mediators produced by certain bacteria which induce dilatation of vessels feeding the extremities: so called, “septic shock.”

How would you propose to treat this disorder?

Please write your answer then open the pop-up card by clicking here.

Pop-up card: Treatment of this condition is ultimately directed at treating the underlying infection. In the meantime, while waiting for the antibiotics to work, you will want to stabilize the patient – create a condition as close to homeostasis as can be achieved. How would you do this? 1. With the dilatation of vessels there is an expansion of the intravascular space, so you will want to expand the intravascular volume in an effort to improve perfusion to tissues. 2. With the dilatation of arteries to the extremities excess blood is unnecessarily shunted there. Consider shunting some blood flow away from the extremities and to critical areas of the body – e.g. to the heart , lungs, brain. The usefulness of using vasoconstrictive agents, such as norepinephrine, is currently quite controversial, but the concept makes sense theoretically and this practice is still widely incorporated into the care of critically ill patients.

Acid/Base Scenario #6:

A 45 year old male has suffered end stage renal disease (ESRD) as a result of long-standing untreated hypertension. He has not been good about keeping his appointments for dialysis and taking his routine medications and presents breathing heavily and feeling very weak.

Background: The body produces a variety of acids as it breaks down food substances in an effort to produce energy and carry out protein synthesis and other cellular functions. When there is normal renal function, the urine is typically acidic as the kidneys dump hydrogen ions in the urine to prevent the accumulation of acid in the body. Additionally, bicarb is lost in the stool on a regular basis. When the kidneys do not function normally, what would you expect to happen to the body’s pH?

So, in the evaluation of this patient with ESRD you obtain routine laboratory tests and get the following results:

ABG: 7.27/24/95/12

Chem: 140 110 56 90

6.8 12 6.4

Osmmeas = 312

What kind of acid/base disorder is this?

Please write your answer then open the pop-up card by clicking here.

Pop-up card: The pH is low, so this is a condition of acidosis. The pCO2 is also low, so this does not explain the acidosis, but instead indicates a compensatory response to the acidosis. The bicarb is low, as expected in a metabolic acidosis, which you already have concluded at this point. Now, the AG = 140 – 110 – 12 = 18, and this is high. The serum Osmcalc = 2 (140) + 90/18 + 56/2.8 = 305. The OG, then, is 312 – 305 = 7, which is normal. So, this is an AGMA with respiratory compensation.

What is the underlying pathophysiology of this disorder?

Please write your answer then open the pop-up card by clicking here.

Pop-up card: The pathophysiology of this case is highly complex, but in its simplest form the patient is regularly producing various acids in the normal process of cellular functions, and since these acids cannot be eliminated by the kidneys, they accumulate in the body and cause acidosis. In reality, many of these acids have sulfate and phosphate anions, and since these anions are not measured and used in the calculation of anion gap, these will be reflected as an anion gap.

How would you propose to treat this disorder?

Please write your answer then open the pop-up card by clicking here.

Pop-up card: Treatment of this disorder is directed at reestablishing homeostasis of the various ions in the blood and achieving a normal pH. This can be accomplished by getting the patient on hemodialysis. A dialysis machine runs the patient’s blood through tubes that come in contact with a solution of electrolytes – the dialysate. The blood and “dialysate” solution is separated only by a semipermeable membrane, so electrolytes and other small particles (e.g. blood urea nitrogen, or BUN) will diffuse freely from one space to another until an equilibrium is established. Since there are no wastes in this solution wastes will flow to the dialysate. Since the patient is acidotic, the blood needs bicarb. In this case, you choose a dialysate that will result in the patient getting a sufficient amount of bicarb. Since the patient’s potassium level is quite high, you will want to choose a dialysate that will bring that down to a normal level as well – using a lower potassium level than usual in the dialysate. There are obviously other medical issues to be concerned with in this highly complex scenario, but for our purposes, what we have covered here accomplishes our objectives.

Acid/Base Scenario #7:

A 37 year old female presents to the ER with severe vomiting and upper abdominal pain. She has been experiencing an “upset stomach” for 3 days and has been drinking bottles of antacids to sooth the pain. She looks pale and weak and has a dry mouth.

You obtain an ABG and a basic chem panel and get the following results:


132 90 28 95

3.0 38 1.0

What kind of acid/base disorder is this?

Please write your answer then open the pop-up card by clicking here.

Pop-up card: The pH is high so this is an alkalosis. The pCO2 is normal so this does not explain the alkalosis and does not indicate respiratory compensation for this disorder. The bicarb level is high, which would be expected in a metabolic alkalosis. This disorder is, then, a metabolic alkalosis.

What is the underlying pathophysiology of this disorder?

Please write your answer then open the pop-up card by clicking here.

Pop-up card: This disorder is the result of acid loss from vomiting and the ingestion of a base (an antacid, typically something related to bicarb, such as Magnesium carbonate). She is also dehydrated, and her BUN/Creatinine ratio reflects this in that it is greater than 20:1.

How would you propose to treat this disorder?

Please write your answer then open the pop-up card by clicking here.

Pop-up card: Treatment of this disorder is directed at the underlying cause, vomiting and ingestion of antacids. The patient first needs to receive IV fluids: a “normal saline” solution with potassium ions in it to get the sodium and potassium levels in the body back to normal. By eliminating vomiting, perhaps with an antiemetic drug (a drug that suppresses the stimulus to vomit), there will be no further loss of stomach acid (HCL). You will also hydrate the patient so the kidneys will filter the blood normally again and reestablish a homeostatic environment with regard to the body’s electrolytes and pH. As long as you can keep the patient from ingesting excessive amounts of antacids, this disorder should be easily remedied.

Acid/Base Scenario #8:

A 19 year old female with history of depression left a suicide post on social media, and now presents with friends after they picked her up and brought her to the ER. She was awake when they got there, but she is now very somnolent. They did bring some empty pill bottles that they found near her at her home. These include acetaminophen, aspirin, citalopram, and hydrocodone/acetaminophen (10/650 mg).

You obtain an ABG and a basic chem panel and get the following results:

7.20/40/75/9 140 105 14 90 EtOH = 0.000

4.0 9 0.9

Osmmeas = 298

What kind of acid/base disorder is this?

Please write your answer then open the pop-up card by clicking here.

Pop-up card: The pH is low and the pCO2 does not explain the acidosis, so this is a metabolic acidosis. The pCO2, though, is not low, so there isn’t the expected respiratory compensation for this acidosis. Further, the AG = 26 (Na+ concentration, 140, minus the sum of the Cl and bicarb, 114), which is elevated. The calculated osmolality is 290, thus there isn’t an abnormal osmolal gap as the OG = 8. This condition, then, is an anion gap metabolic acidosis without respiratory compensation.

What is the underlying pathophysiology of this disorder?

Please write your answer then open the pop-up card by clicking here.

Pop-up card: Aspirin ingestion is the likely culprit causing the anion gap metabolic acidosis. An acute ingestion of acetaminophen does not cause acidosis, but is something that needs to be addressed as it certainly can cause other medical problems (see the Toxicology module). Citalopram is an antidepressant that can cause serotonin syndrome, and in severe cases can contribute to a metabolic acidosis (see Toxicology module for more details). Hydrocodone is an opiate pain medication that can suppress respirations, and is likely the reason why this patient is not compensating for this metabolic acidosis.

How would you propose to treat this disorder?

Please write your answer then open the pop-up card by clicking here.

Pop-up card: This patient clearly has an altered sensorium, most likely from the hydrocodone, to the point respirations are suppressed. A good option in this case would be to reverse the opiate with naloxone and see if she awakens and if her respiratory status improves. If this doesn’t work, or if this is a patient that you are concerned could become violent in the ED if the opiate medication is reversed, you could put this patient on a respirator and admit to the ICU. There is much more to discuss regarding the treatment of aspirin, acetaminophen, and citalopram, but we will hold that for the Toxicology module.


The Renal and GU System covers a vast array of conditions. You are now more familiar with the functions of this system and the lab tests used to diagnose and guide management of related disorders. Interpreting the basic chem panel and blood gas values has carry over to managing disorders of many systems of the body. You have just completed one of the most complex and extensive EMCT modules.


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August 14, 2017

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