McKittrick-Wheelock syndrome - a rare cause of acute renal failure

AIM: Fluid and electrolyte hypersecretion in the villous adenoma of the rectum is presented in the case of a 74 year old man presenting with a severe fluid imbalance. CASE REPORT: The patient had a 2-year history of mucous diarrhea and, on admission, presented prerenal uremia, hyponatremia and severe hypokalemia. At sigmoidoscopy, a 6/4 cm villous adenoma of the rectum was found. The increased loss of volume, followed by exhaustion of the physiological compensation mechanisms, led to a life-threatening hypokalemia, as well as to acute renal failure. Conservative treatment was followed by a temporary improvement of the renal function. Alternative treatment was: endocavitary irradiation, endoscopic resection and radical tumor surgery. The surgical removal of the adenoma led to complete recovery of the symptoms. CONCLUSION: The McKittrick-Wheelock syndrome can be a problem of difficult diagnosis, both for the gastroenterologist and also for the nephrologist. The patient may develop severe complications, which require a sustained treatment.     

A rare cause of fatal right heart failure

Microscopic pulmonary tumor embolism (MPTE) is an uncommon cause of dyspnea in patients with cancer and one of the most difficult to diagnose. MPTE is a syndrome that is pathologically characterized by the occlusion of small pulmonary arteries and arterioles by aggregates of tumor cells. Because the clinical picture resembles that of thromboembolic disease, it is rarely recognized before death. The most common clinical symptom is subacute progressive dyspnea over weeks to months. We recently observed a case of MPTE of exceptional interest as the patient was under aggressive anticoagulant treatment and developed fulminant pulmonary hypertension with fatal right heart failure.     

A rare cause of acute circulatory failure with pulmonary edema: catecholergic cardiomyopathy of pheochromocytoma

We report the case of a 37 years old woman with pheochromocytoma of the adrenal gland, with acute circulatory failure and pulmonary oedema. Its originality lies, besides the rare circumstances of diagnosis, in the echographic aspect of the left ventricle with an apical myocardial infarction with both severe apical hypokinesia and compensating basal hyperkinesia. In the literature the most frequent aspect of catecholamine cardiomyopathy is a large uniform dilatation of the left ventricle with often wall hypertrophy. After surgical ablation of the left adrenal gland tumor, we observe quickly a complete normalisation of the picture and especially the echocardiogram. The cardiomyopathy and the pulmonary oedema can result from the specific action of the excess catecholamines on the myocardial cells and the pulmonary capillaries.     

Amniotic fluid embolism: a rare cause of acute left-sided heart failure

STUDY DESIGN AND SETTING: Two case reports, University Hospital of Antwerp, tertiary referral hospital of the University of Antwerp, Edegem, Belgium. METHODS AND RESULTS: Two women were transferred to our hospital because of acute cardiorespiratory failure due to amniotic fluid embolism during the peripartal period. Both required intensive supportive treatment and invasive monitoring. Haemodynamic data revealed primary left ventricular failure confirming the clinical picture of cardiogenic pulmonary oedema. Review of the literature provides data that do not support obstruction of the pulmonary vasculature by amniotic fluid as the only primary pathophysiological event. However, despite several case reports stressing left ventricular failure as the dominant clinical event, pathophysiological mechanisms are merely speculative. CONCLUSIONS: The diagnosis of amniotic fluid embolism remains a clinical challenge, but can be supported by the presence of amniotic cells in the pulmonary artery, aspirated through a pulmonary artery catheter. The treatment is still not causative but supportive. An overview of cases in the literature with predominant left heart failure during amniotic fluid embolism is given.     

A rare cause of heart failure: hypocalcemic cardiopathy

In this paper, the authors present the case of hypocalcemic cardiopathy observed in a female patient who underwent thyroidectomy which was complicated post-operatively by the development of hypoparathyroidism. Two attacks of heart failure experienced by this patient were improved by the administration of calcium in combination with digitalis treatment. A study of cases published in the medical literature reveals that this condition is a rare cause of heart failure which develops only in the course of chronic hypocalcemia, with few neuromuscular clinical manifestations. The dual negative inotropic and hypovolemic effects caused by hypocalcemia explain the efficacy observed with the administration of calcium therapy, while the usual symptomatic treatment of this condition is inadequate.     

A rare cause of acute appendicitis: parasitic infection

The role of parasitic infection in the aetiology of acute appendicitis has been discussed for more than 100 years. The aim of this retrospective study was to determine the prevalence of parasitic infection in surgically removed appendices, and to identify whether this type of infection is associated with appendicitis. 104 appendices were removed from patients clinically diagnosed with acute appendicitis, and 30 were removed in the course of other surgical procedures. All the operations were performed at Baskent University Adana Hospital between January 1999 and December 2004. Enterobius vermicularis was identified in 4 (3.8%) appendices from patients with clinical appendicitis, and Entamoeba histolytica was detected in 1 (1.0%) appendix from this group. No parasites were found in the 30 appendices that were removed during other surgical procedures. Specimens from 3 of the 4 appendices with E. vermicularis showed no histological evidence of acute inflammation. It is concluded that parasites in the appendix may produce symptoms which resemble acute appendicitis, but parasitic infection rarely causes acute appendicitis.     

Congestive heart failure as cause of fulminant hepatic failure

In this patient with long-standing cardiomyopathy and congestive heart failure the syndrome of fulminant hepatic failure developed on two occasions; he recovered both times. There was no evidence of viral or toxic hepatitis as a cause of his liver failure. We conclude that in this case, aggravation of long-standing congestive heart failure may have led to severe hepatocellular necrosis with signs of encephalopathy not commonly observed.     

A rare cause of acute liver failure- a case report

Background

Acute liver failure (ALF) induced by diffuse metastatic disease has rarely been reported.

Case presentation

We present a 51-years-old woman with relevant clinical history for breast cancer. The patient was admitted in the emergency department with jaundice, dark urine and pale stools. She was on the 10th day of hormonotherapy for recurrence of breast cancer, diagnosed 7 years previously. Usual causes of acute liver failure were excluded, all drugs were stopped and the imaging studies performed were positive only for steatosis. Nonetheless, ALF progressed and the patient died 4 days later. Autopsy demonstrated a massive intrasinusoidal infiltration of the liver by breast cancer cells.

Conclusion

We highlight a rare cause of ALF. Although uncommon, physicians should be alert for this situation as the diagnosis can be challenging and the imaging studies can remain normal.

     

A rare cause of acute abdomen: splenic infarction.

Splenic infarction is a rare disorder. We have treated 4 patients during the last year. Abdominal pain in the left upper quadrant was the common complaint. Other complaints were fever, nausea and vomiting. Computed tomography showed infarcted areas in the spleen in all of the patients. Splenectomy was applied to three of the patients with recurring symptoms. The other patient had the first episode treated medically. Pulmonary embolism in one and surgical wound infection occurred in another patient during postoperative follow-up for nine (range: 4-14) months.