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Biomedical subjects

N Scheffold

Publications and source records attributed to N Scheffold.

16 recordsLinked to original sources

[Isoniazid intoxication].

HISTORY AND ADMISSION FINDINGS: A 55-year-old woman presented with sustained convulsions after the ingestion of an at first unknown amount of isoniazid, rifampin, ethambutol and alcohol. INVESTIGATION: At admission the patient had a severe metabolic acidosis. Blood tests showed changes caused by the hepatotoxicity of isoniazid. TREATMENT AND COURSE: Because diazepam was not efficacious in controlling the convulsions the patient was intubated. In response to the therapautic measures the convulsions stopped and metabolic acidosis was quickly compensated. Pyridoxine was given intravenously as an antidote. CONCLUSION: The rare intoxication with isoniazid demands immediate administration of pyridoxine and aggressive treatment of the convulsions.

Acidosis↗

[Primary diagnosis of an interrupted aortic arch in a 65-year old woman with hypertension].

HISTORY AND PHYSICAL EXAMINATION: A 65-year-old woman presented in a hypertensive crisis and with angina pectoris. She had a history of hypertension for several years and medication included five different antihypertensive drugs. On physical examination a faint systolic murmur was heard. Weak femoral pulses were felt, but not the arterial pulses distal to the groin. INVESTIGATIONS: An attempt to perform coronary arteriography failed because it was impossible to pass the catheter across the aortic arch. MR-angiography and cardiac catheterization via the brachial artery confirmed the diagnosis of a complete interruption of the aortic arch distal to the left subclavian artery and showed distinct collateral circulation predominantly via the internal mammary arteries. DIAGNOSIS AND THERAPY: Because of the age of the patient we assumed that the pathogenesis of this interruption of the aortic arch probably was progression and finally occlusion of an aortic coarctation. It was not possible to distinguish the findings from a true congenital atresia, because there was no histological examination. The patient rejected surgery and conservative therapy with frequent monitoring seemed justified, considering the good blood pressure adjustment and the extensive collateral vascularization. CONCLUSION: Patients with complete interruption of the aortic arch very rarely do reach late adult age without previous surgical intervention. Indeed, such a situation is only conceivable when there is a good collateral blood supply and no concomitant shunt defects. There is an indication for operation, but as there are insufficient follow-up data this should be weighed up carefully in elderly patients whose blood pressure is well controlled.

Aged↗

[Strychnine poisoning].

HISTORY AND ADMISSION FINDINGS: A 46-year-old man presented two hours after ingestion of about 250 mg strychnine with severe violent, generalized convulsions, triggered by external stimuli. During the convulsion-free periods there were no abnormal signs in the physical examination. INVESTIGATION: The presence of strychnine was confirmed by urine analysis with gas chromatography-mass spectrometry. TREATMENT AND COURSE: Because diazepam as anticonvulsant of choice was not effective in abating the convulsions the patient was intubated. A combination with midazolam, fentanyl and pancuronium was effective in controlling the convulsions. The patient was discharged from ICU on day three. CONCLUSION: Fatal outcome of strychnine poisoning demands an aggressive management with early intubation, control of muscle tremors and prevention of rhabdomyolisis and renal failure.

Analgesics, Opioid↗

[Rare complication of a heparin-induced thrombocytopenia type II].

HISTORY AND CLINICAL FINDINGS: A 63-year-old man was admitted to a surgery department with fracture of the acetabulum and luxation of the hip joint. Eight days after intracondylar nail-extension during subcutaneous heparin prophylaxis he developed a dramatic deterioration of his condition with severe abdominal pain and fever and was admitted to our hospital. INVESTIGATIONS: White cell count was 12,000/microliter, C-reactive protein 7.90 mg/dl. CT-scan, abdominal ultrasound, mesenteric angiography and exploratory laparotomy revealed no pathological findings. At day 13 abdominal ultrasound showed adrenal haemorrhages on the right. Together with a drop in platelet count below 50,000/microliter, adrenal haemorrhage caused by heparin-induced thrombocytopenia (type II; immunological [HIT II]) was suggested. THERAPY: After discontinuation of heparin and starting therapy with recombinant hirudin and hydrocortisone, a dramatic clinical recovery followed within 24 hours. One year after the initial diagnosis the patient is in a good condition. CONCLUSION: When abdominal pain, hypotension and fever occurs with a drop in platelet count during heparin therapy HIT II should be considered. An early diagnosis is essential for treatment of this life-threatening complication at an early stage.

Acetabulum↗

[Acute myocarditis and cardiomyopathy in Lyme borreliosis].

Heart involvement of Lyme disease occurs in about 4-10% of patients with Lyme borreliosis. The most common manifestation is acute, self-limiting Lyme carditis, which manifests mostly as transient conduction disorders of the heart, pericarditis and myocarditis. Laboratory tests (ELISA, immunoblotting and PCR) usually have limited sensitivity and specificity, and criteria of performance and interpretation have not yet been fully evaluated. Therefore the laboratory evidence should only be interpreted in conjunction with other clinical and diagnostic features. Recently there has been convincing evidence published that long standing dilated cardiomyopathy in many cases is associated with a chronic Borrelia burgdorferi (BB) infection. Several studies showed a higher prevalence of BB antibodies in patients with severe heart failure in endemic areas (e.g., 26% versus 8% in healthy individuals). The isolation of spirochetes from the myocardium gave further evidence that BB may cause chronic heart muscle disease. In several studies antimicrobial treatment showed an improvement of the left ventricular function in patients with dilated cardiomyopathy associated with BB. However the duration of dilated cardiomyopathy before treatment plays an important part in the clinical outcome of BB-associated chronic myocarditis.

Cardiomyopathies↗

[Intravascular ultrasound in recurrent myocardial ischemia and unremarkable coronary angiogram].

HISTORY AND CLINICAL FINDINGS: 3 months after sustaining an intramural anterior wall myocardial infarction (AWMI) a 57-year-old man was again admitted with the clinical and electrocardiographic (ECG) signs of an acute AWMI. As the activities of creatinine kinase (841 U/l) and of the myocardial isoenzyme (CKMB 143 U/l) were markedly elevated, thrombolysis with streptokinase was instituted. Subsequent left heart catheterization demonstrated discrete wall irregularity in the proximal branch of the anterior interventricular artery (PAIVA) and the right coronary artery, but no evidence of stenosing coronary heart disease. TREATMENT AND COURSE: Because of the discrepancy in the findings, intravascular ultrasound imaging (IVUI) was performed. It revealed an eccentric unstable plaque in the PAIVA with a minimal cross-sectional stenosis of 3.3 mm2 (50% luminal narrowing). After stent implantation under IVUI a good primary result was achieved (stent cross-sectional area 6.2 mm2). CONCLUSION: The usual cause of acute MI is rupture of an unstable, not flow-limiting and thus angiographically possibly "silent" plaque. IVUI can provide immediate assessment of atheromatous wall changes and can thus help to decide on further specific interventional measures.

Cardiac Catheterization↗

[Heparin-induced thrombocytopenia. Diagnosis, clinical course and therapeutic alternatives].

Heparins are common and have been widely used in prophylaxis and therapy of thromboembolic disorders for many years. Nevertheless, the serious side effect of heparin-induced thrombocytopenia type II (HIT II) has attracted attention only recently. First evidence of HIT II is a drop in platelet count below 100,000/mm3. Subsequently, thromboembolic complications occur 6-20 days after beginning heparin therapy. Overall mortality is 20-30% of patients with HIT II. Therefore, frequent platelet counts are required for early diagnosis. However, in cases of moderate or absent thrombocytopenia the diagnosis of HIT II can be difficult. Laboratory tests such as heparin-induced platelet activation (HIPA) test or heparin/PF4-antibody-ELISA have limited sensitivity and specificity. Therefore, with typical clinical findings, divergent laboratory results should be interpreted with caution. If HIT II is suspected, all heparins should be discontinued immediately. Due to a high cross reactivity rate with the heparin-dependent antibody, subsequent therapy with low molecular weight heparins (LMWH) is contraindicated. As treatment of choice danaparoid or recombinant hirudin may be administered. Oral anticoagulation should be started cautiously with an alternative immediate-acting antithrombotic agent. More widespread use of LMWH may reduce the incidence of HIT II in the future. Nevertheless, the main and most important factor in the prevention of this life-threatening complication is the awareness and caution of the clinician.

Anticoagulants↗

[Heparin-associated type II thrombocytopenia as a cause of multiple thromboembolism complications].

13 days after hysterectomy and subcutaneous treatment with unfractionated heparin (10000 IU daily) a 68 year old women developed a pulmonary embolism and deep vein thrombosis of the right leg. She thereupon received intravenous heparin (1000 IU/h). Eight days later she developed acute ischaemia of both legs, and Doppler examination revealed acute Leriche's Syndrome with thrombosis of both iliac arteries. Platelet count fell from, initially 152 x 10(9)/I, to 44 x 10(9)/I. Although heparin-associated thrombocytopenia type II was suspected a confirmation by demonstrating a heparin dependent antibody with the heparin-induced platelet activation (HIPA)-test failed and therefore crossreactivity of low molecular heparins or heparinoids could not be assessed. After discontinuation of heparin and iliacal artery thrombectomy a combination therapy with aspirin plus ticlopidine (500 mg/d respectively) was started and continued until phenprocoumon could exert its full effect. No recurrent thromboembolic events occurred, the platelet counts normalized and the patient fully recovered.

Aged↗

[Metastasizing pancreatic vipoma. Its diagnosis and therapy with the somatostatin analog octreotide].

HISTORY: An 82-year-old woman was hospitalized for anaemia of 4.8 g/dl after having suffered for about one year from watery treatment-resistant diarrhoea, causing a weight loss of ca. 10 kg. FINDINGS: Computed tomography, magnetic resonance imaging and endosonography revealed a 2.5 x 2.0 cm space-occupying mass in the body of the pancreas. Taking into account electrolyte abnormalities (potassium 2.7 mmol/l), marked metabolic acidosis (pH 7.16, base excess -20.3 mmol/l) and achlorhydria, an increased serum concentration of vasoactive peptide (VIP) of 548.5 pmol/l confirmed a VIPoma. Somatostatin-receptor scintigraphy also demonstrated a metastasis, 1.8 cm in diameter, in the region of the right ovary. TREATMENT AND COURSE: Under administration of somatostatin analogue octreotide (150 micrograms three times daily subcutaneously) the symptoms quickly disappeared and the stools as well as electrolyte and acid-base balances became normalized. After 5 months of treatment the levels of VIP, pancreatic enzymes and gastrin were within normal limits or clearly suppressed. There has been no recent evidence of tumour progression. CONCLUSION: This case demonstrates so far successful suppression of a metastasizing VIPoma with the somatostatin analogue octreotide, the metastasis having been revealed first by somatostatin-receptor scintigraphy.

Aged↗

[Intracardial thrombus formation in heparin-associated thrombocytopenia type II].

Deep vein thrombosis of the right leg occurred in a 77-year-old woman after percutaneous cardiac catheterization via the right femoral vein, performed to assess mitral valve disease with atrial fibrillation. She thereupon received intravenous heparin (1,000 IU/h; partial thromboplastin time 60-70s). 13 days later she developed a transient incomplete right brachiofacial hemiparesis with motor aphasia. Transthoracic echocardiography revealed a fresh left atrial thrombus. Platelet count fell from initially normal levels to 20 x 10(9)/l. Because type II heparin-associated thrombocytopenia was suspected heparin administration was discontinued and phenprocoumon administered. Heparin-dependent antibodies were demonstrated with the heparin-induced platelet activation test. Cross reactions occurred in vitro against all low-molecular heparins and heparinoid ORG 10172. The platelet count had become normal 17 days later, the leg veins had recanalized and the intraatrial thrombus had become much smaller. The patient declined cardiac surgery and was discharged on the 41st hospital day in satisfactory general condition on maintenance anticoagulant dosage.

Aged↗

Iodine-123 labelling of atrial natriuretic peptide and its analogues: initial results.

Receptors for atrial natriuretic peptide (ANP) are known to be present in many organs, e.g. brain, liver and kidney. The aim of this study was to optimize the labelling method for ANP analogues with iodine-123 and to describe their pharmakokinetics. ANP 99-126, atriopeptin III, Tyr-atriopeptin II and urodilatin were labelled by the Iodogen method. Of the various labelling conditions tested, the Iodogen procedure with 10 micrograms Iodogen, 10 micrograms peptides in 100 microliters phosphate buffer (pH 7.2) and a reaction time of 60 min proved to be optimal. Separation was performed using a Sep-pak reversed-phase extraction cartridge. In all cases quality control by thin-layer chromatography resulted in a radiochemical purity higher than 98%. After intravenous administration of 15 MBq/kg kinetic profiles of various organs in rabbits were investigated by whole-body scintigraphy with a gamma camera. Organ kinetics showed accumulation and excretion via the kidney. No bowel accumulation was observed. Interestingly, increasing tracer uptake in the head region was registered with three of the four tested tracers. Liver accumulation decreased rapidly during the first 40 min. No tracer degradation was registered over the whole time period, as shown by the low thyroid accumulation with a maximum of only 1%. Thus, labelling of ANF and its analogues is possible. These compounds seem to be of interest for further experiments and perhaps clinical studies because of their potential for brain receptor imaging.

Animals↗

Simplified radiolabeling and initial experimental studies of the in vivo kinetics of iodine-123 atrial natriuretic peptide.

Conventional methods regarding the iodination of atrial natriuretic factor (ANP) were associated with the use of high performance liquid chromatography in a linear elution technique. This chromatographic system is not standard in most radiochemical laboratories. The present study describes a method that allows labeling of ANP with 123I-iodide by using conventional isocratic HPLC equipment. First, the labeled protein was purified in a cascaded way. Then eight gradients with a ratio of acetonitrile/water of 5/95 up to 60/40 (v/v) and a time range of 5 min were applied. The iodinated ANP eluted at about 25 to 30% of acetonitrile. Centrifugation with a speedvac resulted in an injectable solution. Administration of about 20 MBq/kg [123I]iodo-ANP to a rabbit was performed in a pilot study to evaluate the in vivo kinetics of various organs by dynamic acquisition with a gamma camera. The kidneys showed an increasing uptake from 4.2 to 5.3% of total body activity after 75 min. An increasing tracer uptake was also observed in the skull region from 2.4% after 10 min to 3.6% at 75 min. The time activity curve of the liver showed a decrease from 6.6 to 5.1% and that of the heart from 3.7 to 2.9% at 75 min. Thus, labeling of ANP--and probably other peptides--is possible with a simplified cascade elution procedure without the use of gradient HPLC equipment.

Animals↗