Biomedical subjects
Publications and source records attributed to O Pourrat.
We report two cases of severe hypoxemia due to right-to-left shunt in acute asthmatic patients. During acute asthma, the transmural right atrial pressure can be higher than left atrial pressure during inspiration and then induce a right-to-left shunt through inter-atrial communication leading to hypoxemia. Contrast echography as well as Doppler analysis can easily confirm the diagnosis.
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In case of haemolytic uraemic syndrome, it is not always possible to identify on a pure clinical basis the different kidney lesions responsible for the syndrome. We report a series of six cases without thrombotic microangiopathy, which emphasizes the need to perform a kidney biopsy as early as possible, so as to confirm the actual usefulness of plasma exchanges (PE) commonly carried out in emergency in every case of adult haemolytic uraemic syndrome. PATIENTS AND METHODS--Files of patients who were treated for haemolytic uraemic syndrome over the past 14 years were reviewed. Patients in whom thrombotic microangiopathy had been excluded by renal histology data were studied. Every patient was promptly treated with hypotensive drugs, so as to obtain blood pressure levels not exceeding 160-90 mmHg. Dialysis was performed in two patients. Daily PE with fresh frozen plasma were carried out in three patients as early as the first 24 hours after admission, and discontinued immediately after thrombotic microangiopathy could be excluded. RESULTS--All the patients met the usual criteria for diagnosis of haemolytic uraemic syndrome. Elevated liver enzymes were also found in the four cases of preeclampsia, consisting with diagnosis of severe HELLP syndrome. One case was associated with oestrogen therapy. Glomerular lesions were seen in four patients: slight endotheliosis in three cases of preeclampsia; marked lesions of IgA mesangial deposits in the patient who had been treated by contraceptive pill. Three patients had acute tubular necrosis and three had intense lesions of nephrosclerosis. Complete remission was obtained in every case of preeclampsia. Renal failure persisted in two cases (IgA glomerulopathy and one case of nephrosclerosis). DISCUSSION--The histological heterogeneity of haemolytic uraemic syndrome has been already well demonstrated. Typical lesions of thrombotic microangiopathy are usually classified into predominant glomerular lesions, pure arteriolar and mixed lesions. In other cases, thrombotic microangiopathy is not found: kidney lesions may be glomerular (endotheliosis, various subtypes of glomerulonephritis), tubular (acute tubular necrosis) or vascular (nephroangiosclerosis). In every aetiological circumstance, several different lesions may be found together. The usefulness of PE has been proved in thrombotic thrombocytopenic purpura, has been suggested in haemolytic uraemic syndrome and to a lesser extent in persistently severe HELLP syndrome. Unfortunately, none of these reports gave any information about kidney lesions responsible of acute renal failure. CONCLUSION--The haemolytic uraemic syndrome is a syndrome: thrombotic microangiopathy has to be proven when treatment by PE is planned, except in some severe clinical circumstances.
Preeclampsia is a multisystem disorder of pregnancy whose clinical presentation is related to the importance and the extent of maternal microvasculature damage. 16 patients with preeclampsia, thrombocytopenia (< 100,000/mm3), elevated liver enzymes and hemolysis are described. Weinstein in 1982 assigned the acronym of Hellp syndrome for this clinical presentation of preeclampsia. This syndrome was seldom recognized during the first years of the study but was diagnosed later on, in 1 pregnancy out of 600 parturitions and in 5% of preeclampsia in 1991. Two out of the patients developed eclamptic seizures. The mode of delivery was as follows: 9 out of 16 had an emergency Caesarean section; the 7 other patients had vaginal delivery after induction of labor. Delivery occurred before 32 weeks of gestation for 6 out of 17 newborns. Outcome was good for 14 of the 17 newborns (one twin pregnancy). Two fetuses died: one in utero and one during interruption of the pregnancy at 24 weeks of gestation. A small for gestational age preterm of 32 weeks died on his second day of life. Early diagnosis of Hellp Syndrome, especially when abdominal pains are present, allows a prompt management of these patients, including delivery, which appeared in our experience, the only way to avoid fetomaternal complications. The thrombotic microangiopathics and acute fatty liver of pregnancy are potential imitations of Hellp syndrome and they must be considered for differential diagnosis. The frequency of Hellp Syndrome varies from one study to another. It can be increased up to 6 fold if referred to the number of pregnancies and up to 3 fold if referred to the number of preeclampsias. These differences can be real but may be due to bias related to differences in practice between centers and also differences in definitions of Hellp Syndrome and preeclampsia.
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The Hellp syndrome is a complication of raised blood pressure in pregnancy, haemolysis, a rise in liver enzymes and thrombopenia. In this retrospective study we report 12 cases of Hellp syndrome which occurred in the University Hospital Centre of Poitiers between 1982 and 1990 and we discuss causes, the progress, the prognosis and the management. Six patients were helped by prophylactic Caesarean operation. Two patients had eclamptic fits. Fortunately there was no maternal death. There were seven cases of intrauterine growth retardation, two of in utero fetal death and one of early neonatal death. When clinical and biological parameters of the Hellp syndrome come right following delivery, the outlook for the mother is quickly favourable, but the syndrome can continue and sometimes become worse after delivery. Stopping the pregnancy is the basic treatment and conservative treatment has only a very limited success. Finally, the prognosis for the future is usually good and it is unlikely to recur.
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There are similarities between the clinical, biological and histological features of thrombotic micro-angiopathy (TMA) when it is a complication of pregnancy and the "Help Syndrome" (HS). HS can be associated in pregnancy with pre-eclampsia, thrombocytopenia, micro-angiopathic haemolysis and hepatic cytolysis. We have analysed on the one hand biological features of six cases that occurred in the literature and two personal cases of thrombotic micro-angiopathy that had been proven histologically; and on the other hand the histological findings of the liver in two cases of the literature and in a personal case of HS. Demonstration that in HS deposits exist under the endothelium in the region of the hepatic biopsy suggest that the latter can only be a special clinical form of TMA.
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A case of occlusion of the middle cerebral artery during a treatment with gonadotropin is reported. Such cases are unusual when one considers that these treatments are widely used. They occur after a markek ovarian hyperstimulation syndrome. Treatment is purely preventive with clinical, laboratory and ultrasonic examinations before injection of beta-HCG.
In pregnancy pre-eclampsia can be complicated by the nephrotic syndrome. We report on the clinical findings in 23 patients who had the nephrotic syndrome in pregnancy with hypertension. None of these patients had any previous sign of nephropathy. In most patients clinical signs first showed up in the 3rd trimester. The prognosis for the fetus was poor. This was because of the degree of proteinuria and of uraemia (5 fetuses died). After delivery all signs cleared up, as they would have done in moderately severe pre-eclampsia. All patients were considered to be cured by six months. In spite of this the longterm prognosis is difficult to assess. It is necessary to find out whether the nephrotic syndrome was evidence of an underlying nephropathy or just was due to the pre-eclampsia. Treatment consists mainly of rest, control of hypertension, correction of low blood volume and delivery of the fetus with regard to the degree of maturity and the viability of the fetus.
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A 27 year-old alcoholic patient with severe acute pancreatitis (4 Ranson's objective prognostic signs), complained of abdominal pain and vomiting and presented fever and rigors. The plasma was of milky turbidity and the concentration of triglycerides (TG) very high (26 Mmol/l, Normal: 3-1.6). Serum pancreatic amylase was elevated (262 U/l, Normal: 10-200). The electrocardiogram (ECG) showed S-T depression. The diagnosis was confirmed by computed tomography which showed a pancreatic phlegmon and a collection in the left pararenal space (Ranson's grade D). After PE on days 1 and 2: the amylase became normal, plasma clear, TG decreased (7.8 Mmol/l), the clinical picture improved and the ECG normal. Assisted ventilation was necessary over 10 days. Pancreatic morphology remained unchanged. The patient was discharged to intensive care on day 18. There was no indication for surgery. The fast drop in TG levels, the precursors of free fatty acids, may have limited their toxicity the pancreas, allowing a difficult stage to be over come and the course of the illness to interrupted. Normalization of the ECG requires emphasis. The association of HG, increased plasma amylase and abdominal pain justifies early iterative PE.
A patient with myasthenia receiving treatment with anticholinesterase agents and plasma exchanges for an acute episode, developed three successive periods of neurological deterioration during which plasma cholinesterase levels were determined. The risk of onset of a cholinergic crisis under these circumstances has been reported in the literature but not documented. The accidents in the present case were related to cumulative overdose effects of anticholinesterase agents and depletion of cholinesterase, suggesting caution in the use of anticholinesterase agents when frequent plasma exchanges are being carried out in a patient with myasthenia.