Microscopic colitis is characterized by a (near) normal colonoscopy. The diagnosis is established by biopsy of the colonic mucosa. The severity of histological change is most prominent in the proximal colon and declines distally; that is, biopsies from the right or transverse colon are optimal. On histopathology, the condition is separate from collagenous colitis and lymphocytic colitis [1
]. The etiology is multifactorial and it is unknown whether the two subtypes are pathogenetically related [2
]. The peak incidence of the disease is in the age range of 55 to 70 years and occurs predominantly in women (female to male ratio, 2 to 3:1) [3
]. Although most cases are idiopathic, certain drugs can induce the condition, particularly nonsteroidal anti-inflammatory drugs but also acetylsalicylic acid [3
]. Other drugs which can induce colitis include acarbose, ranitidine, sertraline, ticlopidine, flutamide, omeprazole and simvastatin [4
Microscopic colitis may be diagnosed in 10% to 20% of cases investigated for chronic watery diarrhea [2
] of up to two liters per day (four to nine stools daily; sometimes > 10 stools daily). The mechanism of diarrhea in collagenous colitis is believed to be a decreased absorption and increased secretion of sodium and chloride ions [5
]. The absorptive mechanisms of potassium ions are not disturbed by diarrhea per se
, but fecal potassium losses are increased in diarrheal diseases by unabsorbed anions (which obligate potassium loss), by electrochemical gradients secondary to active chloride secretion and probably by secondary hyperaldosteronism [6
When the diagnosis of lymphocytic colitis has been confirmed, the patient's use of drugs and dietary factors that may contribute to diarrhea must be evaluated. Drugs associated with lymphocytic colitis should be stopped. Excessive intake of dairy products, caffeine and alcohol should be reduced. Celiac disease and bile acid malabsorption should be excluded. If symptoms are debilitating, budesonide, a glucocorticoid with low systemic effect due to its substantial elimination by first-pass hepatic metabolism, has been proven effective [7
]. The long-term prognosis for patients suffering from lymphocytic colitis may be more favorable compared to collagenous colitis; diarrhea may subside within weeks with or without treatment and histologic findings may normalize.
In our case, our patient suffered from cardiac arrest due to hypokalemia. The hypokalemia was caused by diarrhea as a consequence of lymphocytic colitis. One case of hypokalemia-induced electrocardiogram changes due to microscopic colitis has previously been reported [8
]. Hypokalemia is a known side effect of budesonide treatment. Our patient stopped budesonide treatment ten days before his cardiac arrest. After his cardiac arrest, our patient resumed budesonide treatment and almost normalized his diarrhea without affecting his serum potassium levels. Following successful resuscitation, no other cause of cardiac arrest could be proven.
Survival from out-of-hospital cardiac arrest is poor [9
]. The interventions linking a patient with cardiac arrest to survival with a good cerebral outcome are known as the chain of survival. This includes early recognition of cardiac arrest, early bystander CPR, early defibrillation and early advanced life support including effective post-resuscitation care. Effective chest compressions with correct chest compression depth and frequency are crucial for a successful outcome [9
This case shows the importance of correcting an underlying cause of cardiac arrest and that survival with a good neurological outcome is possible despite prolonged cardiac arrest.