Necrosis confluent

A 44-year-old woman developed weakness with abnormal liver function tests (aspartate transaminase 661 IU/1) about 6 months after starting to take venlafaxine 150 mg/day. Biopsy showed confluent necrosis in zone 3, with unaffected portal tracts. No other cause for the hepatitis could be found. The clinical and biochemical features resolved within 12 weeks of withdrawal of venlafaxine. 

Clinical features of ARN must include (1) focal well-demarcated areas of retinal necrosis located in the retinal periphery, (2) rapid circumferential progression of necrosis, (3) evidence of occlusive vasculitis, and (4) moderate to severe anterior chamber and vitreal inflammation. Mild presentations may manifest low-grade anterior chamber inflammation with or without blurred vision, whereas severe cases may include episcleritis, scleritis, and pain on eye movement. Early clinical findings include anterior and posterior uveitis, keratic precipitates, and presence of vitreous cells. Within several days to weeks, the patient develops dramatic progressive retinal whitening in multifocal and confluent patches, vasculitis of both retinal arteries and veins, and possible optic nerve head... 

Figure 31-2 Acute retinal necrosis syndrome, with confluent retinal whitening, vitreitis, and vasculitis. (Reprinted with permission from Holland GN, Tufail A, Jordan MC. Cytomegalovirus diseases. In Pepose JS, Holland GN, WUheknus KR, ed. Ocular infection and immunity. St. Louis, MO Mosby, 1996.)...

Confluent necrosis Cell-group necroses can merge within a lobule (= submassive necrosis) or connect affected areas in several different lobules (= multilobular necrosis). 

In persistent confluent and bridging necrosis, the development of correspondingly located fibrotic septa can be observed. Portoportal septa connect neighbouring portal tracts, such as in progressive piecemeal necrosis and in... 

Liver collapse fibrosis must be differentiated from proper liver fibrosis, which displays increased deposition of a qualitatively altered extracellular matrix. It results from a collapse of the reticular fibres following liver cell necrosis. A primary collapse arises subsequent to confluent cell-group necrosis in a previously normal parenchyma. A secondary collapse develops as a result of extensive necrosis in previously damaged parenchyma (e.g. cirrhosis). 

Confluent liver cell necrosis, possibly developing into bridging necroses (32) or multilobular (< 3% of cases) or even massive necroses in B, B/D and C hepatitis, as well as in E hepatitis during pregnancy collapse of the lattice fibre network. Formation of passive septa, cholestasis, accumulation of ceroid and siderin in macrophages and stellate cells. 

Fig. 22.14 Scarred area with fragmented parench)mial islets (- ) after confluent necrosis in the wake of viral hepatitis B (HBsAg+). Localized round-cell infiltration in the remaining parench)Tnal areas (HE)...

A 54-year-old man with rheumatoid arthritis for 12 years was given infliximab, with remission. He then developed a painful, confluent, erythematous, pustular rash over his trunk and limbs. Skin biopsy showed an acute pustular dermatitis. Five hours later he collapsed with a tachycardia (140/minute) and a blood pressure of 120/70 mmHg. He was apyrexial. His left leg was very tense, painful, and swollen, and he had a disseminated intravascular coagulopathy. There was marked necrosis of his adductor compartment and fascia of his left thigh and necrotic muscles were debrided. Blood cultures and skin swabs grew group A hemolytic streptococci. He then became unstable and died, despite efforts at resuscitation. 

The early observations reported for muscle pathology and the associations with mononuclear infiltrates post RRV infection were confirmed by additional studies in mice by Seay and colleagues. Growth was detected in the serum and muscle of 7 day old mice by day 1, with virus detectable in muscle up until day 9 post infection, but only until day 4 post infection in serum, as assessed via plaque assay. In week old mice, foci of muscle necrosis were observed in association with local mononuclear infiltrates at day 5 post infection, which by day 7 post infection saw a prominent mononuclear infiltrate and significant muscle necrosis. In further agreement with previous observations, confluent necrosis and inflammation almost... 

A 21-year-old man took levetiracetam for partial seizures for 1 month, and had a generalized seizure preceded by a 6-day history of pale stools, dark urine, and jaundice. The serum bihmbin was 591 pmol/1, alanine aminotransferase 1610 U/1, alkaline phosphatase 246 U/1, and the international normalized ratio (INR) 3.6. A liver biopsy showed massive confluent hepatocyte necrosis with no evidence of pre-existing liver disease. Levetiracetam was withdrawn but the Uver failure continued to deteriorate and he subsequently required hver transplantation. Postoperatively levetiracetam... 

Skin A serious cutaneous adverse reaction was recently linked to tranexamic acid in a patient with liver cirrhosis and acute rectal bleeding. A 67-year-old male was prescribed oral tranexamic acid, which partially resolved his symptoms. However, 10 days after treatment began a purplish rash appeared on the patient s trunk, which became confluent with blisters and epidermal necrosis over the following days. Tranexamic acid was suspended and a skin biopsy was found to be consistent with toxic epidermal necrosis (TEN). Resolution of the skin lesions was favourable with fluid replacement, oral prednisone and N-acetylcysteine, but after 2 weeks the patient died secondary to acute renal failure, respiratory infection and multiorgan failure. This is the first report of TEN that occurred in a patient being treated with oral tranexamic acid [66 ]. 

The indications and contraindications for laser ablation, and the main complications and methods of follow-up are the same as for radiofrequency ablation and microwave coagulation. The procedures are usually guided with CT or ultrasound although MR is sometimes used as well. By inserting up to eight fibres simultaneously it is possible to achieve confluent necrosis of 6-7 cm in diameter. The ultimate burn size is governed by the tumour vascularity and by the vasodilatory response of surrounding normal liver parenchyma. 

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