Severe Hypophosphatemia Causing Multiple Organ Failure
Bakir, MD, FCCP
Southern Illinois University, school of medicine
Although severe phosphorus depletion can cause malfunctioning of several organ systems, very few cases of multiple organ failure due to hypophosphatemia have been reported.
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.
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.
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.