Acute grade IV toxic hepatitis due to the e-cigarette.

A 46-year-old woman presented at the emergency department because of acute hepatitis with jaundice. After hepatological work-up including liver biopsy, drug induced liver disease (DILI) was suspected. Patient recovered completely within a few months. One year later she presented again with jaundice due to acute hepatitis. Vaping was the only agent that could be identified as causative agent for DILI. After VAPING cessation, the hepatitis resolved completely. Calculated RUCAM score was 10, making the diagnosis of toxic hepatitis very likely. During follow-up liver tests remained normal. This is the first report of severe DILI secondary to the use of e-cigarettes. In future vaping can be included in the differential diagnosis of DILI.

A single-centre analysis of post-colonoscopy colorectal cancer.

PATIENTS AND METHODS: A prospective registration of patients with colorectal cancer and a colonoscopy within the last 10 years. We tried to classify these post-colonoscopy colorectal cancers (PCCRCs) by most reasonable explanation and into subcategories suggested by the World Endoscopy Organization (WEO) and calculated the unadjusted PCCRC rate. RESULTS: 47 PCCRCs were identified. The average age at diagnosis of PCCRC was 73 years. PCCRCs were more located in the right colon with a higher percentage of MSI-positive and B-RAF mutated tumours. The average period between index colonoscopy and diagnosis of PCCRC was 4.2 years. Sixty-eight % of all PCCRCs could be explained by procedural factors. The mean PCCRC-3y of our department was 2.46%. CONCLUSIONS: The data of our centre are in line with the data of the literature from which can be concluded that most postcolonoscopy colorectal cancers are preventable. The PCCRC-3y is an important quality measure for screening colonoscopy. Ideally all centres involved in the population screening should measure the PCCRC-3 y annually, with cooperation of the cancer registry and reimbursement data provided by the Intermutualistic Agency (IMA).

Dysphagia lusoria caused by a right-sided aorta.

We report a case of an 80-year-old female with dysphagia lusoria caused by oesophageal compression by a right-sided atheromatous aorta. The relationship between aortic root vascular anomalies and dysphagia has been clearly established in literature and can be diagnosed by a barium swallowing study, followed by CT or MRI. Aortic anomalies and variations in aortic branches are caused by embryonic malformations and are mostly described in association with congenital heart lesions. In this pauci-symptomatic patient, the preferred treatment is a conservative management.

[Re-expansion pulmonary oedema in a patient after treatment of pneumothorax]. / Re-expansielongoedeem bij een patiënt na behandeling van een pneumothorax.

In a 32-year-old man with left-sided pneumothorax, dyspnoea and tachypnoea with a drop in blood pressure and severe hypoxaemia recurred during drainage. The chest X-ray revealed an alveolar infiltrate in the middle and lower segments of the left lung that was interpreted as re-expansion pulmonary oedema. The patient was respirated and given extra fluids. Extubation was possible after four days. Re-expansion pulmonary oedema is a rare, potentially lethal complication after treatment of a collapsed lung due to a hydro- or pneumothorax. The oedema usually occurs in the re-expanded lung and must be considered when there is a sudden respiratory or haemodynamic deterioration after drainage of X fluid or air. The diagnosis is made by clinical examination and chest X-ray. Predisposing factors are a large hydro- or pneumothorax, long-term collapse, young age and rapid re-expansion. This complication can be prevented by low negative suction pressures and by aspirating a maximum of 1000 to 1500 ml of pleural fluid. The pathophysiology of re-expansion pulmonary oedema is not completely understood and is probably multifactorial. The treatment is merely supportive: oxygen, intravenous fluid substitution and if necessary artificial ventilation. The use of diuretics should be avoided in patients with hypotension.

Hepatocellular carcinoma in Belgium: clinical and virological characteristics of 154 consecutive cirrhotic and non-cirrhotic patients.

OBJECTIVE: This study analyses the characteristics of patients with hepatocellular carcinoma (HCC) in a low endemic area with special emphasis on the differences between cirrhotic and non-cirrhotic patients. DESIGN AND SETTING: The files of 154 consecutive patients with HCC observed in a single tertiary care hospital have been investigated to determine epidemiological parameters and diagnostic procedures. RESULTS: Compared to non-cirrhotic cases, cirrhotic patients with HCC are older and have a more pronounced male predominance. Their disease is more advanced, they usually present with multi-focal tumours, rarely located in the left liver lobe. Antibodies to hepatitis C (anti-HCV) are present in 55%, 52% ever had contact with hepatitis B (HBV) and 31% were hepatitis B surface antigen (HBsAg)-positive. Six non-cirrhotic cases were anti-HCV-positive. alpha-Fetoprotein (AFP) elevation > 50 and > 400 microg/l was more frequently observed in cirrhotic patients with HCC (P = 0.016). A striking association was found between enhanced AFP levels and the presence of anti-HCV (P = 0.0006), while no such relation existed for AFP and HBV markers. The sensitivity of a 'routine' ultrasound examination is disappointing for the early detection of HCC in cirrhotic patients. CONCLUSIONS: In our hospital, in a low endemic area for HCC, we have a surprisingly high proportion of non-cirrhotic patients with HCC (40%). In cirrhosis, usually the consequence of alcohol abuse or hepatitis B or C, small tumours can be missed by ultrasonography if not specifically looked for. AFP levels are particularly elevated in hepatitis C-induced HCC.

Effect of narcotic agents and of bleeding on systemic and renal haemodynamics in healthy and CCl4-treated cirrhotic rats.

1. The haemodynamic effects of different narcotic agents have been tested in healthy rats and in rats with cirrhosis. 2. Pentobarbital suppresses the sympathetic nervous system. Susceptibility to ketamine is unpredictable, leading to both insufficient pain relief and narcosis related mortality. The combination diazepam-fluanisone induces profound hypotension. After insertion of catheters, awake, freely moving rats are stable and not distressed. This allows repeated measurements after manipulation. Moreover, procedure-related mortality is low and rats have a better stress response. 3. In the awake animal, arterial pressure is 126 +/- 10 for healthy animals, and 111 +/- 16 and 102 +/- 10 mmHg for cirrhotic animals without and with ascites, respectively (P = 0.018). The respective values for portal pressure are 6.9 +/- 1.4, 11.6 +/- 2.5 and 16.2 +/- 2.9 mmHg (P = 0.0001). After a bleeding, arterial pressure is better preserved than portal pressure in the three groups (P < 0.0001). Plasma volume in cirrhotic rats exceeds that of healthy rats. Plasma renin activity, aldosterone and catecholamines do not differ between the groups studied. In cirrhotic rats with and without ascites, glomerular filtration rate tends to be higher (P = 0.12), renal plasma flow is elevated (P = 0.001) and filtration fraction is lower (P = 0.002) than in healthy rats. 4. In conclusion, haemodynamic experiments in the cirrhotic rat should be performed in the awake rat. Arterial hypotension, impaired filtration fraction, enlarged plasma volume and portal hypertension are present in cirrhosis before the development of ascites. This can as well be explained by splanchnic pooling of blood, as by peripheral vasodilatation. The decrease in portal pressure with preserved arterial pressure after a bleeding protects cirrhotic rats from ongoing variceal bleeding.

Effects of varying doses of spironolactone without and with nitrates on portal vein pressure and kidney function in partial portal vein ligated rats.

The optimal dose of spironolactone to reduce portal vein pressure, alone or in combination with isosorbide-5-mononitrate (IsMn), has not been identified. We studied the effects of 8 days oral treatment with spironolactone, IsMn or both on portal pressure, plasma volume and renal sodium handling in rats with partial portal vein ligation. At daily doses of 0.33; 0.50; 1, and 1.50 mg/kg, spironolactone reduced portal pressure (all P < .05) as compared with placebo. Only the highest dose significantly lowered plasma volume (10.1 +/- 0.7 vs. 13.0 +/- 0.3 mL; P < .03) and enhanced urinary fractional sodium excretion (0.73 +/- 0.04 vs. 0.58 +/- 0.03%; P < .03) and the (Na+)/(K+) ratio in urine (0.43 +/- 0.04 vs. 0.30 +/- 0.03; P < .02). IsMn at doses of 0.25; 0.50, and 1 mg/kg decreased portal pressure (all P < .05) without a change in plasma volume but with a tendency (not significant) to lower fractional sodium excretion. IsMn impaired free water clearance at doses of 0.5 and 1 mg/kg (P < .05). Combinations of spironolactone 1 mg/kg with IsMn 0.5 or 1 mg/kg have no additive effect on portal pressure compared with spironolactone or IsMn alone. The higher the dose of IsMn in the combination, the more the natriuretic effect of spironolactone is opposed. Low doses of spironolactone are as effective as a higher dose to reduce portal pressure. This reduced portal pressure was independent of changes in plasma volume and diuretic effect, which suggests that spironolactone might have a direct vasoactive effect on the splanchnic circulation. To counteract sodium retention of nitrovasodilators, combination with high doses of spironolactone seems advantageous.

Ascites: medical therapy and paracentesis.

An overview is given of diagnostic determinations to be carried out on ascites fluid, and on the medical therapy as based on our knowledge of the pathophysiology. Paracentesis has become more frequently used. It is slightly more effective than therapy with high doses of diuretics and carries less side effects. Longterm studies are needed to investigate whether albumin can be safely substituted by dextran-70 or haemaccel.

The hepatorenal syndrome.

Hepatorenal syndrome may occur in any form of severe liver disease. It appears less common in children than adults, but still carries a poor prognosis. There are several factors involved in its aetiology, including a decreased renal perfusion pressure, activation of the renal sympathetic nervous system and increased synthesis of several vasoactive mediators, which may modulate glomerular filtration by acting as both renal vasoconstrictors and dynamic regulators of the glomerular capillary ultrafiltration coefficient, through their action on mesangial cells. This review will discuss the pathophysiology of the hepatorenal syndrome and some of the principles of management of patients with renal failure and severe liver disease. The role of renal support and liver transplantation will also be covered.