Acute renal failure following scorpion sting

Fifteen cases of acute renal failure follwoing scorpion sting were studied. The onset of disease was characterized by the occurrence of hemoglobinuria within 24 h of the sting. Most of the patients developed oliguria, edema, hemolytic anemia, and hemolytic jaundice. Renal failure developed within a few days after the sting, and in five patients was severe enough to need dialysis. The onset of diuresis in oliguric patients occurred between 6 and 21 days following the sting. Renal biopsies were possible in four cases and showed mesangial proliferation, variable degrees of tubular changes, and mild interstitial infiltration. The pathogenesis of acute renal failure in these patients is discussed     

Consecutive stings by red scorpions evoke severe cardiovascular manifestations in the first, but not in the second, victim: a clinical observation

Three pairs of scorpion sting victims ((1) daughter and mother, (2) brother and sister and (3) brother and sister) were admitted. In each pair, both were stung by the same scorpion. A patients from each pair were the first stung (initial sting), B patients the second. All A victims of the three pairs had cardiovascular manifestations: hypertension, with pulmonary oedema; hypotension-bradycardia, pulmonary oedema; and hypertension respectively. B victims from the three pairs suffered no systemic or cardiovascular involvement, only severe excruciating local pain at the sting site. It is concluded that A victims received a large dose of venom, injected by the scorpion virtually evacuating the telson resulting in an 'autonomic storm' and severe cardiovascular involvement.     

Scorpion stings in Australia: five definite stings and a review

Despite scorpions being locally abundant in many parts of Australia, scorpion sting is a poorly defined clinical condition in Australia. Many health-care workers are unaware of the effects of their stings and scorpions are often feared based on their international reputation. Five scorpion stings that occurred in different parts of Australia where the scorpion was caught at the time of the sting and identified by a professional arachnologist are reported in the present paper. The spectrum of clinical effects of scorpion stings in Australia and the potential for significant effects are discussed. These cases and recent prospective case series demonstrate that in Australia scorpion stings cause only minor effects. The main effect is localized pain lasting for several hours, associated less commonly with systemic effects, local numbness and paraesthesia. Most stings are from smaller scorpions from the family Buthidae and often occur indoors at night. The stings from Australian buthid scorpions cause more severe effects than from the larger species in the families Urodacidae (genus Urodacus) and Liochelidae (genus Liocheles).     

Prazosin for vasodilator treatment of acute pulmonary oedema due to scorpion sting

Prazosin hydrochloride, a post-synaptic alpha receptor blocking agent, was administered to twelve patients with acute pulmonary oedema due to scorpion sting in order to lower their mean blood pressure (diastolic blood pressure plus one-third of pulse pressure) 10 to 20 mmHg. Following an oral dose (0.125 mg in children and 0.5 mg in adults), clinical improvement was seen in the form of disappearance of apical systolic murmur and pulmonary oedema, a reduction in heart rate observed at the end of the first hour, and maximal improvement seen at the end of the third hour. Chest radiographs showed conspicuous clearing of pulmonary oedema. Electrocardiographs (ECG) showed hypoxic injury patterns such as a Q-wave in lead I and AVL with tented T waves in precordial leads, left anterior hemiblock (LAHB) and acute infarction patterns with subsequent T-wave inversion. The severity of clinical signs and ECG changes increased as the time between the sting and attending hospital lengthened.     

Insulin reverses haemodynamic changes and pulmonary oedema in children stung by the Indian red scorpion Mesobuthus tamulus concanesis, Pocock.

The efficacy of insulin administration in reversing haemodynamic changes in pulmonary oedema in victims of poisonous scorpion sting is assessed by a study based on animal experiments in which insulin administration reversed metabolic and electrocardiographic changes induced by scorpion envenomation. Six previously healthy children aged 18 months to 11 years were admitted to hospital five to 17 hours after scorpion sting. Frusemide for raised central venous pressure and pulmonary oedema, crystalloid infusion for reduced central venous pressure, and hydrocortisone and dopamine for hypotension were used as standard therapy. Insulin (0.3 units g-1 of glucose) was administered when the standard therapy failed to produce an improvement, and at the earliest sign of haemodynamic instability. Reversal of pulmonary oedema and haemodynamic changes, and attainment or normal respiratory rate, blood pressure and central venous pressure, were observed. It is concluded that insulin administration may be useful in reversing haemodynamic changes and pulmonary oedema in victims of scorpion stings.     

Myocardial damage with life-threatening arrhythmia due to a scorpion sting

Yellow scorpion venom is known to evoke cardiovascular responsesand cause severe myocardial damage in man. Life-threateningarrhythmias in such cases are rare. This work describes twosuch cases, and discusses the problems posed by ventriculararrhythmias in cases of scorpion sting.     

Scorpion sting-induced pulmonary edema. Scintigraphic evidence of cardiac dysfunction

We report two cases of pulmonary edema due to scorpion sting. Radionuclide ventriculography (MUGA scan) showed localized cardiac dysfunction. The cardiac injury induced by the scorpion venom persisted for a prolonged period.     

Cholinergic hypothesis of alcoholic pancreatitis.

Chronic alcohol intake interferes especially with the two main pathways regulating exocrine pancreatic secretion: the cholinergic and the pancreozymin pathway. Recently, a new theory of the pathogenesis of alcoholic pancreatitis was proposed emphasizing disordered agonist-receptor interaction at the level of pancreatic acinar cells. Accordingly, alcohol-induced alterations in the control of exocrine pancreatic secretion result in hyperstimulation of pancreatic acinar cells and their muscarinic receptors, mimicking the mechanism of acute pancreatitis caused by scorpion sting, intoxication with an anti-acetylcholinesterase-containing insecticide or supramaximal doses of secretagogues. The present review emphasizes the role of these alcohol-induced secretory alterations in the pathogenesis of alcoholic pancreatitis.     

The electrocardiographic changes in patients stung by scorpions

Scorpion sting is a hazardous and potentially lethal condition. Venom of some variety of scorpion can cause dramatic cardiovascular and electrocardiographic changes, that have been related to heart stimulation by autonomous nervous system. We prospectively studied 722 patients following scorpion sting. Mean age for the group was 25.5 +/- 18.3 years. 67% were less than 30 years of age. In 294 patients (40.7%) we found electrocardiographic changes. These cases were followed until those changes disappeared. First degree atrioventricular block was found in 10.2%. Intraventricular conduction disturbances in 12.8% with predominance of right bundle branch block. In 11% we found arrhythmias. In 15% reversible ventricular repolarization changes. Of this no one died. This lack of mortality could be attributed to a prompt therapeutic intervention.     

Treatment of cardiovascular manifestations of human scorpion envenoming: is serotherapy essential?

Death due to sting by the red scorpion is not uncommon in parts of India. Extensive clinical study has shown that fatality is due to cardiovascular involvement as a result of autonomic storm. Prazosin and nifedipine helped to counter the physiological actions of scorpion venom on the sympathetic nervous system. Scorpion antivenom remains unobtainable for human scorpionism in India.     

Role of atropine in management of cardiovascular manifestations of scorpion envenoming in humans.

We undertook a retrospective analysis of 35 victims of red scorpion (Mesobuthus tamulus) sting, admitted to our hospital in Mahad, Maharashtra State, India. Increase in duration as well as severity of clinical signs, including myocardial injury and poor response to conventional treatment, were observed in 17 victims treated with atropine compared to another 18 victims who were not so treated. We do not advocate routine use of atropine to block transient cholinergic effects of scorpion envenoming.     

The haemolytic-uraemic syndrome in childhood

Haemolytic-uraemic syndrome (HUS) is a clinical syndrome characterized by acute haemolytic anaemia with fragmented erythocytes, thrombocytopenia and acute renal failure. It is one of the leading causes of acute renal failure in childhood. HUS in children can be divided into the so-called typical, diarrhoea-associated HUS, and atypical HUS, which is not preceded by acute gastroenteritis. Infection with verocytotoxin-producing Escherichia coli is the main cause of diarrhoea-associated HUS. In this chapter the pathogenesis of diarrhoea-associated HUS and the role of verocytotoxin-producing Escherichia coli in this form of HUS is emphasized.     

Androctonus crassicauda sting and its clinical study in Iran

Androctonus crassicauda is the second most frequent cause of scorpion sting in southwest Iran. Its toxin can cause severe pain, autonomic, CNS, and muscle function disturbances, and death. Appropriate medical and nursing care can lead to complete recovery with no sequelae.     

Das hämolytisch-urämische Syndrom im Kindesalter

Hemolytic-uremic syndrome (HUS) is among the most common causes of acute renal failure in childhood. A heterogenous group of diseases with varying etiology and clinical course, HUS is characterized by Coombs-negative acute hemolysis, thrombocytopenia, and acute renal failure. Histologically, all forms have thrombotic microangiopathy in common. In terms of therapeutic options and prognostic factors, it is reasonable to differentiate between classic diarrhea-associated (D+) HUS and atypical HUS not associated with diarrhea (D? HUS). In childhood 90% of all cases are D+ HUS, with a more favorable prognosis, whereas the prognosis in D? HUS is rather poor. Although many underlying causes for different D? HUS forms have been identified in the last few years, for many cases the pathogenesis remains unclear. In the following we discuss etiology, prognosis, and therapeutic options for the different forms of HUS.     

Enhanced proteolysis of plasma von Willebrand factor in thrombotic thrombocytopenic purpura and the hemolytic uremic syndrome

To examine whether enhanced in vivo proteolysis of von Willebrand factor (vWF) would account for the reported loss of larger multimers in acute thrombotic thrombocytopenic purpura/hemolytic uremic syndrome (TTP/HUS), we studied eight patients with acute TTP/HUS whose blood samples were collected into an anticoagulant containing a cocktail of protease inhibitors to impede in vitro proteolysis. In all, enhanced proteolytic degradation of vWF was expressed as a relative decrease in the intact 225-Kd subunit of vWF and a relative increase in the 176-Kd fragment. However, instead of the loss of larger forms of normal multimers reported by other investigators, the plasma of all but one of our patients (whether they had TTP or HUS) contained a set of larger than normal (supranormal) multimers. Hence, although proteolytic fragmentation of vWF was enhanced during acute TTP/HUS, this phenomenon was not associated with the loss of larger multimers. In the five patients who survived the acute disease and underwent plasma exchange (three with HUS and two with chronic relapsing TTP), subunits and fragments returned to normal values, and supranormal multimers were no longer detected in plasma. In conclusion, even though vWF proteolysis is enhanced in acute TTP/HUS, it does not lead to loss of larger multimers.     

Abnormal VIII: von Willebrand factor patterns in the plasma of patients with the hemolytic-uremic syndrome

Plasma VIII:von Willebrand factor antigen (VIII:vWF) levels were elevated approximately two- to eightfold in seven patients (three adults and four children) during acute episodes of thrombocytopenia, renal failure, and hemolytic anemia (the hemolytic-uremic syndrome, HUS). In all seven patients, there was an alteration in plasma VIII:vWF patterns during these acute HUS episodes, so that the largest VIII:vWF forms were relatively decreased. Plasma VIII:vWF multimer patterns returned to normal, or nearly to normal, as platelet counts returned to preexisting levels, even in the patients whose recovery of renal function was incomplete and whose plasma VIII:vWF antigen level remained above normal. The sister of one of the HUS patients had a similar clinical prodrome (gastroenteritis) that was not followed by thrombocytopenia or renal failure and was not accompanied by an elevated level or abnormal forms of plasma VIII:vWF. These results suggest that an alteration in VIII:vWF metabolism, distribution, or interaction with platelets is associated with acute HUS episodes. In contrast to patients with chronic relapsing thrombotic thrombocytopenic purpura, none of the HUS patients (either during or after the acute HUS episodes) had a defect in the conversion of unusually large VIII:vWF multimers derived from endothelial cells to the VIII:vWF forms found in normal plasma.     

Therapeutic apheresis in the treatment of hemolytic uremic syndrome in view of pathophysiological aspects

Hemolytic-uremic syndrome (HUS) is a disease that can lead to acute kidney injury and often to other serious sequelae, including death. The disease is characterized by microangiopathic hemolytic anemia, thrombocytopenia, and acute kidney injury. In view of the different courses of HUS, a minimum of three different pathogenetic types leading to HUS can be subdivided as follows: HUS caused by infection, idiopathic HUS (non-Shiga toxin HUS), and HUS in systemic diseases and after toxin exposure. The etiology and pathogenesis of HUS are not completely understood and its therapy is complicated. After the introduction of therapeutic apheresis as a supportive therapy in HUS, several authors reported successful treatment in more than 87% of treated patients. The supportive therapy is indicated basically in severe courses of HUS and is superior to available therapy interventions.     

Hemolytic-uremic syndrome as a presenting form of acute lymphocytic leukemia

 We report an 8-year-old girl who presented with hemolytic–uremic syndrome (HUS) as the onset manifestation of acute lymphocytic leukemia (ALL). The patient was admitted to the hospital for renal failure, thrombocytopenia, and anemia during a HUS outbreak. She was discharged 2 weeks later with normal renal function. One month later the girl presented with clinical and laboratory signs consistent with a diagnosis of ALL. The short time interval between HUS and ALL suggests that HUS was probably an early manifestation of acute leukemia. Received: 13 April 1999 / Accepted: 9 February 2000     

Hemolytic uremic syndrome by Streptococcus pneumoniae

Hemolytic uremic síndrome (HUS) is an acute disease characterized by microangiopathic hemolytic anemia, thrombocytopenia, and acute renal failure, usually,but not always, associated with the prodrome of diarrhea. A 2-year-6-month old boy with pneumonía caused by Streptococcus pneumoniae developed the third day after admission oliguric acute renal failure, anemia, and thrombocytopenia. The patient needed veno-venous hemodiafiltration/ hemofiltration during ten days. He received five packed red blood cell, and one platelet transfusions, and was treated with plasma infusions during six days. Renal function was normal at discharge. HUS caused by Streptococcus pneumoniae has more morbility and mortality that classic HUS, although they usually recovery renal function. In those cases of atypical HUS, different from others, blood transfusions that contains IgM should be avoided,because they can increase antigen-antibody reaction and cellular damage. The low incidence of HUS by Streptococcus pneumoniae and the systemic infectious component difficult the early diagnosis. Taking into account the different transfusion approach in these cases, it is necessary to be aware for diagnosing HUS by Streptococcus pneumoniae in all patients with systemic infection and sudden renal function deterioration.     

Hemolytic uremic syndrome

Hemolityc anemia, thrombocytopenia and acute renal failure are characteristic features of hemolytic uremic syndrome (HUS). The disease occurs mainly in infants and little children, sometimes it occurs in adult people. Most often it occurs in the course of diarrhorea cause by E. coli O 157:H7. Many other agents can induce HUS. The case of 54 year old female with HUS which developed in the course of diarhoea was reported. The course of HUS was complicated by multiorgan--brain, heart, pancreas and liver injure. Hemodialysis and plasmapheresis were used in the treatment. The treatment made the health recovery possible in our case.