It's all about the lemon juice...

At Renal Grand Rounds last week one of our fellows, Dr. Martina McGrath, presented the case of a 53 year old male with no past medical history, who initially presented with fever, chills, chest pain and epistaxis, was diagnosed with acute pericarditis and was noted to be pancytopenic. Further workup and ultimately bone marrow biopsy was diagnostic for AML and he was transferred to our tertiary care hospital to commence induction chemotherapy.

His course was remarkable for pericarditis and tamponade necessitating pericardial drain placement. After a repeat bone marrow biopsy was complicated by large pelvic hematoma he developed transfusion dependent anemia, necessitating more than 10 units of PRBCs. Unfortunately, he developed worsening bilateral pulmonary infiltrates necessitating BiPAP support and total body ECF volume overload ensued. This necessitated daily furosemide to control his volume overload.

A renal consult was called because he developed metabolic alkalosis with the following laboratory results:

Na-126 K-5.0 Cl-87 CO2-38 BUN-17 Creat-0.58 Glucose-119

Ca-8.4 Phos-2.6 Urate-2.8 Alb-2.8

ABG:pH-7.53 pO2-67 pCO2-48

ALT-61 AST-52 Alk phos-150

Hgb-8 Hct-25 WBC-7.5 Plts-28

The chest xray showed severe bilateral airspace disease consistent with pulmonary edema.

What is the acid base abnormality and why?

It is clear that this patient had metabolic alkalosis with relatively appropriate respiratory compensation, depending on how closely correlated these laboratory tests are in time.

Metabolic alkalosis is a relatively common clinical problem, most often induced by diuretic therapy, or the loss of gastric secretions due to vomiting or nasogastric suction.

Two separate abnormalities can contribute to metabolic alkalosis:

1. An elevation in the plasma bicarbonate concentration due to hydrogen loss in the urine or gastrointestinal tract, hydrogen movement into the cells, the administration of bicarbonate, and contraction alkalosis.
2. A decrease in net renal bicarbonate excretion.
   

In this patient, contraction alkalosis and loss of chloride and hydrogen ions in the urine due to diuretic therapy was certainly a contributor. However, another important consideration was his exposure to a large amount of bicarbonate infused into his body in the form of citrate, given normal liver function. We often forget about iatrogenic factors in our patients, but in this case, his multiple blood transfusions were certainly an important source of citrate/bicarbonate.

Metabolic alkalosis has been described:

• The infusion of more than eight units of bank blood (anticoagulated with citrate).
• Observed when citrate rather than heparin was used as an anticoagulant in hemodialysis
• Continuous renal replacement therapy (CVVHD) with citrate.
• Extensive use of crack cocaine (which contains significant amounts of an alkali) in dialysis patients.
• Fresh frozen plasma as a replacement fluid during plasmapheresis.