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SEVERE HYPOPHOSPHATEMIA CAUSING MULTIPLE ORGAN FAILURE
M. Haitham
Bakir, MD, FCCP
Southern Illinois University, school of medicine
Introduction
Case Presentation
Discussion
Conclusion
Although severe phosphorus depletion can cause malfunctioning of several organ systems, very few cases of multiple organ failure due to hypophosphatemia have been reported.
Top
A 60-year-old
white woman with a history of alcoholism and chronic obstructive pulmonary
disease was transferred from an outlying hospital for management of
respiratory failure.
She had a two-week history of cough, fever, progressive shortness
of breath, generalized weakness and confusion.
Physical examination revealed an unresponsive malnourished patient
on ventilator support. Temperature was 39.1 C. Lung exam showed rhonchi
and decreased breath sounds in the right lung. The rest of the exam
was unremarkable.
White blood count was 14,600 with left shift. The hemoglobin was 7.4
Mg/Dl, MCV of 81 and reticulocyte count of 2.8. Peripheral smear showed
schistocytes and spherocytes. CK was 10,241.
Chest X-ray showed consolidation in the right upper lobe and cardiomegaly.
Her arterial blood gas showed metabolic acidosis (pH of 7.25, pCO2
of 38, PaO2 of 96 and bicarbonate of 16). Sputum culture was positive
for Streptococcus pneumoniae. Blood cultures were negative.
Echocardiography showed severe global cardiomyopathy with an ejection
fraction of 24% (previous ejection fraction 1 year ago was 40%). Because
the patient’s unresponsiveness persisted since the admission
lumbar puncture and computerized tomography of the head were normal.
Serum phosphate was 0.3 mg/dl (normal range: 2.5-5). Intravenous phosphorus
replacement was started at 2.5 mg/kg over 6 hour’s doses. Approximately
30 hours later the patient became responsive. Her ventilatory parameters
improved and she was extubated 36 hours after phosphorus replacement
was started. The creatine kinase normalized. She persisted with marked
muscle weakness and required several weeks of physical therapy. She
was discharged on hospital day 32.
Top
This is a unique case because
the patient has the complete constellation of clinical manifestations
associated with severe hypophosphatemia: respiratory failure, cardiomyopathy,
rhabdomyolysis, coma, hemolysis, myopathy, metabolic acidosis, and
even being prone to sepsis.
It is believed that most of the clinical manifestations of hypophosphatemia
are due to depletion of intracellular adenosine triphosphate (ATP)
and decreased 2, 3 dyphosphoglycerate in erythrocytes (reducing oxygen
release at the tissue level).
Also severe hypophosphatemia reduces both phagocytosis and granulocyte
chemothaxis and predisposes to infection.
Alcoholic patients admitted to intensive care units are at increased
risk due to previous poor nutritional status, the use of phosphate
binder antacids, vomiting and diarrhea. Urinary phosphate excretion
also tends to be increased in these patients.
Use of carbohydrate infusions like 5% dextrose will produce a phosphate
shift from serum to the cells, contributing to low serum levels.
Intravenous replacement should be used only in symptomatic patients
with phosphorus levels less than 1 mg/dl and can reverse rapidly the
clinical consequences.
Top
1- hypophasphatemia should
be suspected in every alcoholic patient with respiratory failure.
2- If initial phosphorus level was borderline normal should be repeated
after giving dextrose solution.
3- Severe hypophosphatemia can cause reversible multiple organ failure.
Top
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Page Last Updated September 12, 2008