Electrolyte imbalances: are all the same?

Introduction: We present the case of a 72 year-old woman admitted with a diagnosis of diverticulitis in April 2012 to our surgical department for severe diarrhea. An abdominal CT scan confirmed a diverticular disease of the sigmoid colon with multiple protrusions, inflammatory imbibition of perivisceral fat and mesenteric lymphadenopathies. Later the patient developed vomiting, weakness with postural instability, and cachexia with weight loss of 9 kg. For the progressive worsening of her clinical conditions she was transferred to our Internal Medicine Department, in the critical care area. History: The patient was affected by systemic hypertension and chronic kidney disease (CKD) with moderate secondary normochromic anemia. She was submitted 13 years before to left nephrectomy for renal carcinoma and, 12 years before, to hemicolectomy for ascending colon cancer. She was taking angiotensin receptor blockers (ARBs), allopurinol, statins, D vitamin and subcutaneous erythropoietin. She wasn’t currently taking any proton-pump inhibitor (PPIs). Laboratory: At the admission to our department, we observed a neutrophilic leukocytosis, mild normochromic anemia, renal failure, increased indices of inflammation and hyperuricemia; liver and thyroid function were normal. Urinary electrolytes were at the lower limit. Vidal–Wright reaction, ruling out Salmonellosis and Brucellosis, was negative as well as a stool cultures, occult fecal blood and the research of parasites and C. difficile toxins. However, the presence of a faecal calprotectin[300 and the presence of persistent diarrhea and increased ESR and CRP raised the suspicion of an inflammatory bowel disease, having excluded a celiac disorder. Following Procedures: Colonscopic examination with biopsies showed only signs of inflammation in preanastomotic area due to edema, and chronic nonspecific signs of inflammation at the biopsy. After the colonoscopy, the patient presented stupor, and tonic–clonic seizure with fever. An electrolyte imbalance was suspected as a possible cause of this complication: severe hypomagnesemia (0.4 mg/ dl), hypocalcemia (5.9 mg/dl) and hypokalemia (2.9 mEq/l) were found. The immediate administration of intravenous MgSO4 (4 g e.v. in 24 h) and liquids allowed the complete resolution of neurological symptoms. We also observed a normalization of diarrhea and electrolytes in the following days. Therefore, the diarrhea has assumed a dual role: as cause and effect of an electrolyte imbalance. The patient was discharged in good general conditions with calcium and magnesium oral supplements. Conclusions: This case highlights an often underestimated, often misleading clinical entity, such as electrolyte imbalances. On this subject there is very little in the literature. Electrolyte homeostasis is integrated and the normalization of a parameter can not be obtained without the infusion of another electrolyte. In our case, hypomagnesemia and hypocalcemia. Acute hypomagnesaemia the less frequent imbalance, often diagnosed with delay (magnesium is not routinely evaluated). In addition, it rarely occurs as an undeferrable urgency or with a definite clinical picture, as in this case; symptoms are often non-specific and common to many other diseases. Chronic hypomagnesemia is closely related with hypocalcemia, which is caused by impaired parathyroid hormone (PTH) secretion or the refractoriness of bone and renal tubules to PTH. The dominant mechanism of acuteonset, hypomagnesemia-induced hypocalcemia is currently unclear [1]. Another cause of hypomagnesemia is the adverse effects of longterm proton pump inhibitor therapy, but our patient was not taking PPIs [2]. The guidelines, algorithms, protocols, show us the way forward, and are a good ‘‘cookbooks’’, but remember that the patient is always in need of a thinking chef