A case of neuroleptic malignant syndrome with acute renal failure]

Neuroleptic malignant syndrome is a potentially lethal side effect of neuroleptic drugs, characterized by fever, muscle rigidity, autonomic dysfunction, and altered consciousness. A 50-year-old female hospitalized three times in the past for psychiatric treatment was admitted to Umayabashi Hospital for treatment of a relapse of a schizophrenic psychosis. She had received 50 mg of chlorpromazine and one tablet of Vegetamin-A (chlorpromazine 25 mg, promethazine 12.5 mg, phenobarbital 40 mg). Approximately 24-36 hours later, the patient became febrile and lost consciousness, and eight days later, acute renal failure occurred with muscle rigidity. She was transported to Maebashi Red Cross Hospital to receive hemodialysis. On admission, the laboratory studies showed high levels of serum creatine phosphokinase, glutamic oxaloacetic transaminase, glutamic pyruvic transaminase, creatinine and blood urea nitrogen. She underwent hemodialysis for treatment of acute renal failure and recovered from it after 16 sessions of hemodialysis.     

Successful treatment of six patients with neuroleptic malignant syndrome associated with myoglobulinemic acute renal failure

Neuroleptic malignant syndrome is a rare but potentially lethal, rare reaction to neuroleptics which is characterized by altered levels of consciousness, extrapyramidal effects, autonomic instability, hyperthermia, and elevated serum creatine phosphokinase levels. The most serious complication of neuroleptic malignant syndrome is acute renal failure. We investigated six cases of neuroleptic malignant syndrome associated with myoglobulinemic acute renal failure due to rhabdomyolysis and effect of hemodialysis or hemodiafiltration. The patients were five males and one female with a mean age of 43.5 yr. All of the patients, who developed acute renal failure induced from rhabdomyolysis, had previously received butyrophenone (haloperidol), phenothiazine, benzamide, iminomide, benzisoxazole, antidepressants, and hypnotics (benzodiazepine and barbiturate) for the treatment of schizophrenia. The clinical manifestations of neuroleptic malignant syndrome were characterized by altered consciousness, muscle rigidity and weakness, fever, and excessive perspiration. The peak laboratory data were blood urea nitrogen 102 +/- 26 (mean +/- SD) mg/dL, serum creatinine 9.1 +/- 2.1 mg/dL, serum creatine phosphokinase 229,720 +/- 289,940 IU/L, and all of them developed oliguric acute renal failure. Dantrolene sodium administration was given to five cases and hemodialysis or hemodiafiltration was performed in all of them. The serum creatinine level after hemodialysis or hemodiafiltration was 1.4 +/- 1.0 mg/dL. All patients were successfully cured of acute renal failure by hemodialysis or hemodiafiltration. As a result, myoglobulinemic acute renal failure associated with neuroleptic malignant syndrome was successfully treated by hemodialysis or hemodiafiltration.     

Plasmapheresis in neuroleptic malignant syndrome

Neuroleptic malignant syndrome is a severe and potentially fatal reaction to neuroleptic drugs. Treatment requires withdrawal of the neuroleptic agent, metabolic and cardiovascular support, physical cooling and treatment with dantrolene sodium and bromcriptine mesylate. We report a therapeutic success of plasmapheresis in a case of neuroleptic malignant syndrome in which conventional therapy had failed. We postulate that plasmapheresis may prove to be a useful tool in treating this frequently fatal disease.     

The neuroleptic malignant syndrome

Following the administration of fluphenthixol (a depot phenothiazine) for a psychotic illness, a 44-year-old woman developed weakness, rhabdomyolysis and renal failure, together with hyperthermia (42 degrees C) and signs of both autonomic and central nervous system dysfunction. She died following massive intestinal haemorrhage, intra-abdominal sepsis and probable disseminated intravascular coagulation. A diagnosis of neuroleptic malignant syndrome had been made, but treatment with dantrolene sodium was probably instituted too late to prevent the progress of the complications she had developed. This syndrome, which follows the use of phenothiazines or butyrophenones, is rare, potentially fatal and probably underdiagnosed. It has been likened to malignant hyperthermia, but a review of the literature points to many differences. Both dantrolene sodium and dopaminergic drugs (bromocriptine, amantidine and L-dopa) have been shown to be efficacious and their continued use, despite a failure in this case, is advocated until more is known about this syndrome.     

Neurogenic bladder in neuroleptic malignant syndrome

Urinary retention or incontinence is not an infrequent clinical finding in patients with neuroleptic malignant syndrome. We studied the pathophysiology of this voiding disorder by urodynamic testing. It revealed involuntary bladder contraction and rigidity of external sphincter (dyskinesia). These findings are analogous to those in Parkinson disease patients and support the dopamine deficiency theory as the cause of neuroleptic malignant syndrome.     

The malignant neuroleptic syndrome and malignant hyperthermia

We report on a patient with neuroleptic malignant syndrome (NMS) caused by a therapy for endogenous depression. The symptoms were hyperpyrexia (39.2 degrees C), rigidity, elevated creatine kinase (CK: 594 U/l) and coma. After transfer from an outside hospital, he was treated, at first without effect with dantrolene p.o. (80 mg q.i.d.) and i.v. (1 mg/kg-1/h-1). Clinical improvement and temperature reduction were noted when the levels of neuroleptic drugs fell during unspecific intensive care with mechanical ventilation, sedation (flunitrazepam, barbiturates), relaxation (pancuronium), and hydration. After uncomplicated weaning from the ventilator the patient became more cooperative and was returned to the psychiatric ward. Further treatment took the form of combined drug therapy with biperiden and flunitrazepam and in addition a series of 12 electroconvulsive therapies (ECT). The elevated CK levels initially decreased, serum potassium levels were found to be within normal limits, and myoglobinuria was not detected during the further course. Trigger agents for NMS are antipsychotic drugs such as thioxanthenes, phenothiazines and butyrophenones. Because the signs and symptoms are so similar to those of malignant hyperthermia (MH), it has been suggested that NMS and MH are related diseases. The postulated mechanisms of NMS become apparent in the CNS, whereas those of MH affect the muscle cell itself. An abnormal in vitro contraction test after NMS should suggest to triggering of MH crisis after succinylcholine administration in anaesthesia for ECT.(ABSTRACT TRUNCATED AT 250 WORDS)     

Acute renal failure due to malignant lymphoma infiltration

We present two cases of renal lymphoma revealed by acute renal failure (ARF), which remains a rare clinical entity. Case 1 was a 29-year-old man with an ARF. The diagnosis was a primitive kidney immunophenotype B lymphoma. The patient died after three courses of chemotherapy due to rapid spread lymphoma. The second case was a high-grade renal lymphomatous infiltration, with an unusual computer tomography image of two large kidneys compressing the stomach. Death happened early before initiating therapy. In both cases the diagnosis has been established by renal pathology. Early diagnosis is a key component of therapeutic success, however, the rapid spread of lymphoma worsened renal and vital prognosis.     

Malignant hyperthermia susceptibility in neuroleptic malignant syndrome

The relationship between neuroleptic malignant syndrome (NMS) and malignant hyperthermia (MH) was investigated using the in vitro skeletal muscle contracture test to screen for MH-susceptibility in NMS patients. The maximum contracture tension which developed following exposure to halothane (1-3%), and incremental doses of fluphenazine (0.2-25.6 mM) was measured in muscle obtained from seven NMS, six MH, and six control patients. Comparison of the cumulative responses to fluphenazine revealed no significant differences among the groups. However, the response (mean +/- SEM) to halothane in the NMS group (1.7 +/- 0.7 g), which was similar to the response in the MH group (1.5 +/- 0.2 g), was significantly greater than the response found in controls (0.2 +/- 0.1 g). In addition, five of seven NMS patients could be diagnosed as MH-susceptible, based on the development of muscle contractures greater than 0.7 g in response to 1-3% halothane. In contrast, none of the controls were MH-susceptible. These findings appear to correlate with clinical evidence suggesting an association between NMS and MH.     

Acute renal failure due to crush syndrome

Summary The clinical and pathological aspects in 23 cases of acute renal failure (ARF) due to crush-compression are presented. The chief findings are oliguria or anuria, usually occurring within 48 hours of trauma, and severe uremia, hyperkalemia and elevation of muscle enzymes. The mortality in this series was 30,4%, most commonly due to infectious complications. Treatment principles are aggressive debridement, early dialysis and, when clinically indicated by lack of response to these measures, amputation of the crushed extremity.     

Acute renal failure due to HELLP syndrome and acute renal failure in mid gestation

A 34-year-old grand multipara (para 7, 4 alive) was managed at the National Hospital, Abuja, Nigeria for acute renal failure due to HELLP syndrome following referral from a peripheral hospital. She presented with a history of vomiting, headache, epigastric pain, loss of consciousness and tonic/clonic seizures. Though she was unsure of her exact dates, clinically the gestational age was estimated at 22 weeks. She was managed in the intensive care unit, following delivery of a macerated fetus within 15 h of hospital admission. The patient received mechanical ventilation and three sessions of haemodialysis as part of her successful management while in the intensive care unit. The uncommon presentation of eclampsia and HELLP syndrome before obvious preeclampsia is discussed, as well as the other signs and symptoms and patient management. The case also highlights the resource-poor environment of peripheral and tertiary hospitals in Nigeria.     

Acute renal failure in a patient with hemophagocytic syndrome

Acute renal failure (ARF) occurred in a 47-year-old man with hemophagocytic syndrome. Histological findings of the kidney revealed diffuse infiltration of interstitium by phagocytosing cells mixed with atypical lymphoid cells of varying size. The cytological features of the lymphoid population in liver and spleen were consistent with a diagnosis of peripheral T-cell lymphoma. We believe that this ARF could have been exacerbated by the interstitial infiltration of phagocytosing cells, reactive lymphoid cells, and T-cell lymphoma cells. Received: September 25, 1998 / Accepted: July 22, 1999     

Acute renal failure in children with idiopathic nephrotic syndrome

Acute renal failure (ARF) is an uncommon but alarming complication of idiopathic nephrotic syndrome. The renal failure could be secondary to causes evident from the history and evaluation, such as severe intravascular volume depletion, acute tubular necrosis, allergic interstitial nephritis, bilateral renal vein thrombosis, acute pyelonephritis, or rapid progression of the original glomerular disease. It may be termed idiopathic if the underlying cause is undetermined. We present three children with idiopathic nephrotic syndrome who were admitted with acute renal failure. One case was due to drug-induced allergic interstitial nephritis. The other two were idiopathic in nature. Improvement in renal function occurred in the three patients over a variable period of 10 days to 4 weeks. After careful exclusion of well-known causes of acute renal failure, idiopathic acute renal failure (IARF) should be considered as a diagnostic possibility in these patients. The exact pathophysiology of IARF is not understood. Possible proposed explanations include interstitial edema, tubular obstruction, altered glomerular permeability, and unrecognized hypovolemia.     

Acute renal failure due to severe Landry-Guillain-Barre syndrome

Background: Blood urea nitrogen (BUN) >60 mg/dl has been reported to occur commonly in patient's with severe Landry-Guillain-Barré syndrome. Aims: To find out the cause for this high BUN we compared the renal function tests of 30 consecutive cases with severe Landry-Guillain-Barré syndrome to those of 30 controls. Results: Acute renal failure occurred in seven patients with Landry-Guillain-Barré syndrome and one of the control group. Acute renal failure was found more in cases with Landry-Guillain-Barré syndrome compared to controls (P=0.0049). Six out of seven cases with Landry-Guillain-Barré syndrome and acute renal failure had dysautonomia and became oliguric while being in a hypotensive state. Of 30 patients with Landry-Guillain-Barré syndrome seven cases died. From eight patients with dysautonomia six cases who had acute renal failure died. The mortality rate was higher in cases with dysautonomia and acute renal failure (P=0.0001 and 0.00001, respectively). Interestingly no glomerular disease was found. Conclusion: In conclusion acute renal failure can occur commonly in cases with severe Landry-Guillain-Barré syndrome particularly in those with dysautonomia, causing high mortality.