Dark Urine - Case 20-3: 10-Year-Old Boy
I. History of Present Illness
A 10-year-old boy who was previously well developed rhinorrhea with cough and
intermittent fever 1 week before admission. For the 4 days before admission, he
complained of severe myalgias, followed by weakness and the inability to walk.
His urine had become cola-colored, but he had not had any dysuria or increased
frequency. He had had no emesis or diarrhea, and he had not complained of
headaches. He was initially admitted to a community hospital, where his liver
function tests and creatine kinase (CK) concentration became dramatically
elevated. His CK more than doubled in 12 hours, and he was then transferred to
an academic center.
II. Past Medical History
He had never been hospitalized and had had no surgeries, and he had never before
experienced the presenting symptoms. His family history, however, was
remarkable. Both his father and a paternal first cousin had similar episodes
when they were about 20 years old. The family had recently emigrated from
Trinidad.
III. Physical Examination
T, 38.9°C; RR, 20/min; HR, 68 bpm; BP, 120/60 mm Hg; SpO2, 100% in room air
On examination, the patient was in mild distress but was well hydrated. There
was no scleral icterus or mucosal pallor. His neck was supple, and his lungs
were clear to auscultation bilaterally. His cardiac examination was normal, and
the capillary refill time was less than 2 seconds in all of his extremities.
His abdomen was benign. His thighs, calves, and arms were all tender. He was
able to move his extremities, but only with extreme pain. When pressed, it
appeared that his strength was intact. His cranial nerves appeared to be intact
as well.
IV. Diagnostic Studies
The patient had a normal electrolyte panel, including a potassium concentration
of 4.5 mEq/L and a creatinine level of 0.8 mg/dL. His hepatic function panel
was remarkably abnormal: total bilirubin, 0.4 mg/dL; albumin, 3.6 mg/dL;
alkaline phosphatase, 274 U/L; ALT, 720 U/L; and AST, 3,480 U/L. His
prothrombin and partial thromboplastin times were normal. A urinalysis was
significant for 3+ protein and 4+ blood. However, there were minimal red blood
cells on microscopy. An electrocardiogram showed normal sinus rhythm. Lactate,
pyruvate, plasma amino acids, acylcarnitine, urine organic acids, total and
free carnitine, and ketones were all evaluated.
Discussion: Case 20-3
I. Differential Diagnosis
Hemoglobin or myoglobin most commonly causes cola-colored urine. This patient's prodromal respiratory illness led to consideration of postinfectious
glomerulonephritis, although the time course between the prodrome and the
urinary changes was short in this case. Respiratory symptoms have also been
associated with exacerbation of IgA nephropathy and benign recurrent hematuria,
but this patient had never experienced these symptoms before. In addition, the
lack of red blood cells on microscopic analysis supported diagnoses consistent
with free hemoglobin or myoglobin. He had no other symptoms of sepsis, so
diffuse intravascular coagulation syndrome was unlikely. The patient
's severe myalgias brings to mind rhabdomyolysis, but an inciting cause would
need to be identified. Trauma, strenuous exercise, prolonged seizures,
hyperthermia, and toxins such as cocaine or neuroleptics have been associated
with rhabdomyolysis, but this patient did not report any of these exposures.
True polymyositis is exceptionally rare in children and is usually more
chronic. Influenza has been associated with myositis, especially of the
gastrocnemius muscle, and it is a rare cause of true rhabdomyolysis. The family
history indicated the possibility of a heritable susceptibility to
rhabdomyolysis.
II. Diagnosis
The patient's initial CK value was 100,000 U/L, and it ultimately rose to 690,000 U/L. The
myocardial bound (MB) fraction was only 26 U/L, making a cardiac cause
unlikely. In conjunction with the elevated AST on the hepatic function panel,
the diagnosis of rhabdomyolysis was made. The family history made a form of
autosomal dominant rhabdomyolysis likely, although no specific defect was found
in this case. A heritable defect of the mitochondrial respiratory chain is the
most likely metabolic defect leading to myoglobinuria in the setting of a
febrile illness.
III. Incidence and Epidemiology
The incidence of rhabdomyolysis is difficult to define because it has a variety
of causes (Table 20-2). Autosomal dominant rhabdomyolysis has been reported in
the literature only a handful of times. A Swiss family was described in 1997 in
which 10 individuals experienced myoglobinuria in the setting of a febrile
illness. A variety of pathogens were identified, including
Escherichia coli, Streptococcus pneumoniae, Epstein-Barr virus, and influenza B virus. Four of the patients had received
general anesthesia without incident, and none of the family members had
experienced exercise-induced myoglobinuria. A specific mutation was not
identified in this family, but muscle biopsy in the index case was consistent
with a disorder of cytochrome c oxidase in the respiratory chain. Mutations in
the ryanodine receptor have been implicated in some cases of malignant
hyperthermia caused by anesthesia. Fatty acid oxidation defects may put some
patients at risk for exercise-induced myoglobinuria.
IV. Clinical Presentation
Clinical symptoms specific to rhabdomyolysis consist of a classic triad that
includes myalgias, weakness, and dark urine. Myalgias may be severe enough that
the patient is unable to walk. On examination, the patient
's muscles are tender to palpation. Associated symptoms depend on the cause.
Signs and symptoms of shock may accompany trauma, burns, or severe dehydration
from strenuous exercise or heat shock. A postictal state is seen after a
prolonged seizure. Mental status changes are seen with many of the toxins
listed previously. Diabetic ketoacidosis is preceded by a period of polyuria,
polydipsia, and polyphagia. Crush injuries are the presenting complaint in
patients who have experienced this kind of trauma, and the pain from the actual
injury obscures the more general symptoms of the developing rhabdomyolysis.
V. Diagnostic Approach
Urinalysis. Urine dipstick tests are positive for blood, but microscopy reveals no red blood
cells.
Creatine kinase. CK becomes dramatically elevated, peaking 24 to 36 hours after the onset of
rhabdomyolysis. There is no significant elevation of the MB fraction.
Electrolytes and minerals. Potassium and phosphate can become dramatically elevated because of high muscle
content spilled into the extracellular compartment. Calcium may drop secondary
to the rapid rise in phosphate.
Electrocardiography. If hyperkalemia is present, an electrocardiogram is critical for monitoring the
potential for a life-threatening arrhythmia. Peaked T waves are seen, with
potassium levels greater than 7 mEq/L. As levels rise above 8 mEq/L, P waves
are lost and the QRS widens. At a level of 9 mEq/L, there is further QRS
widening and ST-segment depression. Levels greater than 10 mEq/L lead to
bradycardia, first-degree atrioventricular node block, and, ultimately,
ventricular dysrhythmias and cardiac arrest.
Renal function tests. A rising blood urea nitrogen and creatinine concentrations indicate impaired
kidney function, presumably because of precipitation of myoglobin in renal
tubules.
VI. Treatment
The inciting event should be identified and, if possible, eliminated. All other
elements of therapy are aimed at facilitating the clearance of myoglobin, to
prevent renal failure, and preventing severe hyperkalemia. If there is evidence
of shock (e.g., crush injury, burns, heat stroke, severe exertion), boluses of
isotonic saline in aliquots of 20 mL/kg should be used to restore adequate
perfusion. Intravenous fluids are then used to maintain a brisk urine output of
at least 4 mL/hr. There should be no potassium in this stock solution.
Bicarbonate needs to be added to the intravenous fluids, with the goal of
maintaining a urine pH greater than 7. This minimizes precipitation of
myoglobin in the kidneys.
If urine output falls, a dose of Lasix (furosemide) can be tried to prevent
oliguric renal failure. This may, however, make it more difficult to alkalinize
the urine, because the kidney will retain bicarbonate to maintain anionic
balance in the face of chloride loss caused by Lasix.
Hypocalcemia may be seen with rhabdomyolysis, so supplemental calcium may be
required. Severe hyperkalemia needs to be managed aggressively to prevent an
arrhythmia. Kayexalate (sodium polystyrene sulfonate) is a potassium-binding
resin that is given by mouth. It is one of the few ways to actually remove
potassium from the body. A dose of 1 to 2 g/kg is given with 3mL of sorbitol
per gram of resin. Potassium shifts intracellularly in an alkaline environment,
so sodium bicarbonate can be used to acutely lower serum potassium levels.
Insulin also drives potassium into cells. It should be given as 0.1 U/kg but
must be accompanied by 2 mL/kg of 25% dextrose given over 30 minutes to avoid
hypoglycemia. Dialysis is the last resort in the face of renal failure and
hyperkalemia.
VII. References
1. Brumback RA, Feeback DL, Leech RW. Rhabdomyolysis in childhood. Pediatr Clin North Am 1992;39:821–858.
2. Chamberlin MC. Rhabdomyolysis in children: a 3-year retrospective study. Pediatr Neurol 1991;7:226–228.
3. Cronan K, Norman ME. Renal and electrolyte emergencies. In: Fleisher GR,
Ludwig S, eds.
Textbook of pediatric emergency medicine, 4th ed. Philadelphia: Lippincott Williams & Wilkins, 2000:811–858.
4. Martin-Du Pan RC, Morris MA, Favre H, et al. Mitochondrial anomalies in a
Swiss family with autosomal dominant myoglobinuria.
Am J Med Genet 1997;69:365–369.
Pictures
Book Source Details
- Book Title: Pediatric Complaints and Diagnostic Dilemmas
- Author(s): Samir S Shah MD; Stephen Ludwig MD
- Year of Publication: 2003
- Copyright Details: Pediatric Complaints and Diagnostic Dilemmas, Copyright © 2003 Lippincott Williams & Wilkins.
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Copyright Details: Pediatric Complaints and Diagnostic Dilemmas, Copyright © 2008 Williams & Wilkins.
More About Causes of Darkened urine
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