Treatment of severe thallium intoxication.

CASE REPORT: We report a successfully treated case of severe thallium intoxication. In spite of very high serum thallium (5,240 micrograms/L), symptomatology was minor and recovery complete. Prussian Blue was administered, diuresis was enhanced by intravenous fluids and a prolonged hemodialysis was started early. High blood flows (300 mL/min) and intravenous potassium chloride supplements, to mobilize thallium from the tissues, resulted in good clearances (96 to 150 mL/min). In order to prevent the well known complications, we recommend aggressive treatment of severe thallium intoxication.

Acute renal infarction and heavy marijuana smoking.

The first case of acute renal infarction in a patient with heavy marijuana smoking is described. The patient had no concomitant previous medical history. There was no evidence of a primary or secondary hypercoagulable state. Underlying neoplasm was excluded. Recovery was associated with normalization of transaminases and lactic dehydrogenase but with a persistent triangular hypoechogenic area in the right kidney. The combination of marijuana-associated alterations in systemic blood pressure due to peripheral vasodilation, functional anemia and an adrenergic effect might have been the cause of the arteria renalis thrombosis in our patient, but the real underlying pathophysiological mechanism still remains unresolved.

Acute renal failure due to bilateral lymphomatous infiltrates. Primary extranodal non-Hodgkin's lymphoma (p-EN-NHL) of the kidneys: does it really exist?

Primary extranodal non-Hodgkin's lymphoma (p-EN-NHL) of the kidneys with acute renal failure as the only manifestation is very rare. The origin of neoplastic lymphoid cells in the kidneys, organs normally free of lymphoid tissue, is an unsolved problem. A literature review over the last ten years revealed only 9 adult cases, including ours that match the usual criteria: (1) renal failure as the initial presentation, (2) bilateral enlargement of the kidneys without obstruction and other organ or nodal involvement, (3) diagnosis only made by renal biopsy, (4) absence of other causes of renal failure, and (5) rapid improvement of renal function after radiotherapy or, as in our case, systemic chemotherapy. Autopsy on two patients confirmed that p-EN-NHL of the kidneys without dissemination does exist as a separate entity.

Orthodeoxia and platypnea in liver cirrhosis: effects of propranolol.

Chronic liver disease is well known to be associated with pulmonary abnormalities. Hypoxemia, clubbing, cyanosis and hyperventilation are common. The hypoxemia in cirrhotic patients has several causes: diffuse shunts due to intrapulmonary arteriolar vasodilatation, impaired hypoxic vasoconstriction, impaired matching of ventilation to perfusion, pleural effusions and diaphragmatic dysfunction. Because of gravity, shifting of blood to the dilated precapillary beds of the lung bases results in an increased hypoxemic dyspnea when the patient is in the upright position, also known as orthodeoxia and platypnea. It has only been described in 5% of the cirrhotic patients and has not been described in a Belgian refereed journal (Medline literature search 1983-Aug 1993). It should be considered in the initial differential diagnosis of hypoxemia in patients with liver cirrhosis and dyspnea. Measuring arterial blood gases in the lying and upright position can prevent further invasive investigations, and whole body nuclide scan with technetium-99m macroaggregated albumin can confirm the diagnosis. Standard therapy with spironolactone (Aldactone) can worsen the condition and we found no additional benefit of beta-antagonists (propranolol/Inderal) in the reduction of the shunt fraction, probably because the main reason for the shunting is precapillary vasodilatation. Since there are no anatomical porto-pulmonary shunts, surgery is also inappropriate. The only therapy consists of oxygen supplements and low dose diuretics in patients with edema.

Filum terminale ependymoma revealed by acute cauda equina compression syndrome following intratumoral and spinal subarachnoid hemorrhage in a patient on oral anticoagulants.

A 65 year-old woman with a filum terminale ependymoma is reported, presenting with acute cauda equina compression syndrome due to intratumoural and subsequent spinal subarachnoid hemorrhage (SAH) following therapy with oral anticoagulants. Few cases of spinal ependymoma have been reported with an acute cauda equina compression syndrome as the initial and only symptom, and the unique feature of our patient's anticoagulant status has only been described once in this setting. Although intratumoural hemorrhage is very well known since the myxopapillary variant is unique to the cauda equina and consists of loose connective tissue and numerous small blood vessels that are prone to bleeding, spinal SAH is seldom seen and the different hypotheses about the pathophysiological mechanisms that might promote bleeding still remain unresolved and will be discussed in this paper, as well as the special clinical features of spinal SAH and some diagnostic and therapeutic implications. A review of the literature (Medline search 1983-1993) revealed only 13 cases, including ours, of spinal SAH due to cauda equina ependymoma, and the results of this review together with our findings are described in this paper.

Intranasal caffeine and amphetamine causing stroke.

A 37 year-old man with an ischaemic stroke after the nasal use of amphetamine and caffeine is reported. Transient arterial hypertension due to these agents may have been the mediator of the stroke. Mitral annular calcification was the only other abnormality found, and was thought not to play an important role in this patient. There was no evidence of a primary or secondary hypercoagulable state. Stroke due to nasal use of these agents appears not to have been previously reported (Medline literature search 1983-1993).