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Case 14 – A 68-year-old man with lower abdominal pain

A 68-year-old man presents to the emergency department with severe lower abdominal pain. He has a constant desire to urinate but can only produce a small amount of urine. His past medical history is unremarkable, but he says he has experienced hesitancy before the onset of urination and decreased strength of his urinary stream for several months. Physical examination is significant for trace pedal edema, and his blood pressure is 140/86 mm Hg, with no orthostatic changes. He has marked tenderness in the suprapubic region and dullness to percussion to the level of the umbilicus. Rectal examination reveals a large, smooth, firm, midline mass located anteriorly. Laboratory tests show:

Sodium: 142 mEq/L
Potassium: 6.0 mEq/L
Chloride: 113 mEq/L
Bicarbonate: 17 mmol/L
Blood urea nitrogen: 110 mg/dL
Creatinine: 7 mg/dL
Hemoglobin: 15 g/dL
Hematocrit: 45%

What is the most likely cause of this patient’s lower abdominal pain?

This is an example of post-renal (obstructive) acute renal failure. The patient’s early symptoms are suggestive of a partial bladder outlet obstruction. His current symptoms suggest that the obstruction is essentially complete. The suprapubic tenderness and dullness to percussion are due to a distended bladder. These signs and symptoms in elderly men are most commonly caused by benign prostatic hyperplasia, but prostate cancer must also be considered.

How do the laboratory findings help to confirm the diagnosis?

The elevations in blood urea nitrogen (BUN) and creatinine levels indicate a significant reduction in glomerular filtration rate (GFR). This is due to the increased tubular hydrostatic pressure from the obstruction, which offsets glomerular capillary hydrostatic pressure. The BUN:creatinine ratio is increased because of decreased flow through the collecting duct, which causes enhanced urea reabsorption. The normal hemoglobin and hematocrit levels indicate that this is acute and not chronic renal failure, which almost always causes a hypoproliferative anemia.

How could this diagnosis be confirmed?

A catheter bypassing the obstruction may be placed in the bladder. This is sometimes difficult to do when the prostate is very enlarged. An ultrasound of the kidneys would show dilated renal collecting ducts and bilateral ureteral dilatation. A bladder scan would show a markedly enlarged bladder.

What is the most appropriate management for this patient?

Temporary relief may be achieved with a transurethral catheter, if possible. A suprapubic catheter should be considered if the prostate is too large to pass a catheter by. A transurethral prostatectomy is the definitive procedure. In addition, a work-up to distinguish benign from malignant prostatic disease should be conducted.

What are potential consequences of the treatment?

A postobstructive diuresis is typical after the relief of prolonged urinary tract obstruction. The magnitude of the diuresis can reach several liters per day. One mechanism for this is due to the elimination of sodium and water retained during the period of obstruction. Once the obstruction is removed, GFR increases and the excess sodium and water can be eliminated, which is a self-limiting process. Another mechanism is osmotic diuresis from retained urea, which is eliminated as GFR recovers.

By Kristen Vierregger, University of Pennsylvania School of Medicine, Class of 2008; in association with Le TT, Schabelman E, Shivaram A, and Klein J, eds: First Aid Cases for the USMLE Step 2 CK. New York: McGraw-Hill, 2007.

Case 13 – A 70-year-old man with narcotic overdose

A 70-year-old man with a history of chronic obstructive pulmonary disease (COPD), congestive heart failure (CHF), myasthenia gravis, and chronic back pain is recovering after a motor vehicle accident. The patient fractured both tibiae and multiple ribs, but remains without serious internal organ injury. His problem during this hospitalization has been pain control. He has recently been transitioned to oral oxycodone, but morphine injections are still being used for breakthrough pain. At the 4 a.m. vital sign check, the night nurse notes the patient is unarousable. He has a respiratory rate of 5/min and an oxygen saturation of 80% by pulse oximetry. His heart rate is 80/min and blood pressure is 130/80 mm Hg. He has pinpoint pupils, a normal cardiac examination, and clear lung fields. Arterial blood gas analysis shows a pH of 7.02, partial pressure of carbon dioxide of 90 mm Hg, partial pressure of oxygen of 45 mm Hg, and bicarbonate of 15 mEq/L. Administration of 100% oxygen via a non-rebreather mask raises the oxygen saturation to 95%. Review of the medication logs shows that the patient accidentally got two morphine boluses in addition to his maximum oxycodone dosage.

What is the most likely diagnosis?

Acute hypercarbic respiratory failure secondary to narcotic overdose. Opiates depress the central drive to breathe, first causing hypercarbia and then hypoxia. Some of the other causes suggested by the patient’s history include COPD or asthma exacerbation, flash pulmonary edema secondary to CHF, or respiratory muscle weakness due to myasthenia gravis. However, the clinical picture of decreased mental status, depressed respiratory rate, and overmedication suggest narcotic overdose.

How is the diagnosis approached?

The first step should be an arterial blood gas analysis. This will differentiate between hypercarbic or hypoxemic respiratory failure. Pure inhaled oxygen should also be administered. If this improves oxygenation, the pathology is due to ventilation/perfusion (V/Q) mismatch. If oxygenation does not improve, a shunt physiology is suggested.

How is the A-a gradient calculated and what is its significance?

The A-a gradient is the difference between alveolar and arterial oxygenation. It is calculated as:

[(PATM ? 47) × FIO2] ? [(PAO2 ? PACO2 / 0.8)]

A normal A-a gradient is 5-10 mm Hg. An increased gradient indicates a problem getting alveolar oxygen into the bloodstream. Hypoventilation alone results in hypoxemia with a normal A-a gradient.

What other conditions should be included in the differential diagnosis?

The differential list for acute respiratory failure is very broad and can be divided into two categories: hypercarbic and hypoxemic. Hypercarbia is caused by decreased ventilation, due to loss of central drive (secondary to toxins or brain stem injury) or respiratory muscle failure (due to myasthenia gravis, Guillain-Barré syndrome, or botulism). Hypoxemia that corrects with oxygen therapy can be due to V/Q mismatch, often due to intrinsic lung disease such as COPD, asthma, interstitial lung disease, or a pulmonary embolus. Hypoxemia due to shunt physiology can be the result of a true vascular or intracardiac shunt; severe alveolar filling as seen in pneumonia, pulmonary edema, or hemothorax; or alveolar collapse as seen in COPD or asthma.

What is the most appropriate management for this patient?

The underlying disease process must be addressed; in this case, naloxone should be given to reverse the effects of the narcotics. Oxygenation can be improved by increasing FIO2 and adding positive end-expiratory pressure in a mechanically ventilated patient. Hypercarbia is controlled by changing minute ventilation (increasing respiratory rate and/or tidal volume).

By Melissa Rosenstein, MD, Resident in Obstetrics, Gynecology and Reproductive Sciences, University of California, San Francisco Medical Center; in association with Le TT, Schabelman E, Shivaram A, and Klein J, eds: First Aid Cases for the USMLE Step 2 CK. New York: McGraw-Hill, 2007.