Angioneurotic oedema

It is usually recommended that ACE inhibitors be continued peri-operatively in common with other antihypertensives. There is some evidence that postoperative haemodynamic stability is improved and renal function protected. Pretreatment with ACE inhibitors may reduce tachyphylaxis to sodium nitroprusside and help to prevent rebound hypertension. On the other hand, there is evidence that ACE inhibitors may predispose to hypotension during anaesthesia and that they reduce cerebral blood flow during any period of systemic hypotension. Furthermore, the response to and recovery from hypotensive episodes due to blood loss or circulatory depletion may be impaired. At present, the advice concerning these drugs would be to continue therapy up to and including the day of operation. Another rare side-effect of ACE inhibitors is angioneurotic oedema, which has occasionally been seen complicating intubation. 

Several cases of serious and even fatal intoxication after dermal application of resorcinol have been described. Methaemoglobinaemia, haemolysis and convulsions have often been noted (Cunningham, 1956 Lundell Nordman, 1973 Bontemps et al., 1995). Resorcinol is a rare cause of allergic contact dermatitis (Vilaplana et al., 1991 Pecegueiro, 1992 Serrano et al., 1992 Massone et al., 1993) and may also induce generalized eczema, urticaria and angioneurotic oedema (Barbaud et al., 1996). 

Andre F, Veysseyre-Balter CE, Rousset H, Descos L, Andre C. Exogenous oestrogen as an alternative to food allergy in the aetiology of angioneurotic oedema. Toxicology 2003 185 155-60. 

Baars JW, Wagstaff J, Hack CE, Wolbink GJ, Eerenberg-Belmer AJ, Pinedo HM. Angioneurotic oedema and urticaria during therapy with interleukin-2 (lL-2). Ann Oncol 1992 3(3) 243. ... 

Srivastava S. Angioneurotic oedema following atracurium. Br J Anaesth 1984 56(8) 932-3. 

Nomura S, Hashimoto J, Osawa G. Can Cl esterase inhibitor concentrate be a cause of the exacerbation of hereditary angioneurotic oedema Vox Sang 1995 69(1) 85. 

This dye, paraphenylenediamine, when mixed with henna, blackens the hair in a very short time. The substance is a common cause of ATN in the Sudan [30]. It is also toxic to the heart and hver. It is absorbed through the skin but individuals have ingested the dye in suicide attempts. Within 3-4 hours after ingestion they develop angioneurotic oedema soon followed by renal failure. Renal biopsy shows the typical features of acute tubular necrosis. See chapter 40. 

The experience of PPD intoxication in children is even worse. A reported series of 31 Sudanese children between 1984 and 1989, all children presented with acute and severe angioneurotic oedema, 15 required tracheotomy. ARF was reported in 5 children and the mortality rate was 41% and most children died within the first 24 hours. [27]. In another report of Wad Medani teaching hospital 2.6% from their series were children and the common cause of poisoning was accidental [25] (Figure 4). Statistics from the ENT teaching hospital in Khartoum from 1995 to 2005 showed that of 3159 patient admitted with PPD intoxication 568.6(18%) were children below the age of 14 years. In a report from the poison control centre of Morocco, PPD intoxication was reported in 43 (11.5%) children below the age of 15 years. [21]... 

Little is known about the mechanism of inflammatory pain. Kelly has discussed the question of pressure on nerves. The accumulation of exudate in an abscess leads to pain which is immediately relieved when the abscess is incised. On the other hand, greater tension exists in tissues affected by angioneurotic oedema although no pain is produced. It is known that externally-applied pressure, insufficient to elicit pain in normal tissue, causes pain in an inflamed area. Randall and Selitto used this hyperalgesic state as the basis for their now widely used test for analgesic drugs. 

This evidence suggests that enkephalinase inhibitors may produce adverse effects similar to ACE inhibitors such as angioneurotic oedema and persistent cough which have been linked to suppression of bradykinin deactivation [139,140,141]. 

Individuals with hereditary angioneurotic oedema lack serum CT-esterase inhibitor, the inhibitor of the activated first component of hemolytic complement. During an acute episode of this disorder circulating CT-esterase, which is a permeability-increasing factor in human skin, is markedly increased [57, 97, 140, 142, 219, 332]. It is unlikely that a similar mechanism is involved in the anaphylactoid reaction in rats as reactivity is not an absolute phenomenon [32-34, 274]. The final inflammatory mediator(s) of the reaction is, therefore, available for release in both reactor and non-reactor rats. This implies that the trigger mechanism or some intermediary step in the reaction is different in the two types of rat. 

This is an or2 Slobulin which limits the action of Cl, the first complement component. A genetic defect in the synthesis of Cl esterase inhibitor occurs in l reditary angioneurotic oedema. Cl esterase inhibitor can be measured immunochemically or by its ability to inhibit the hydrolysis of synthetic esters by a preparation of activated Cl. 

The first case of angioneurotic oedema due to oral thiamine administration has been reported [24 ]. 

Osman M, Casey P. Angioneurotic oedema secondary to oral thiamine. BMJ Case Rep September 19,2013 2013. pii bcr2013200558. 

A double-blind trial against placebo was carried out in 50 obese patients over a 12-week period (25 ). Six patients failed to complete the 12-week course. Four of these were in the placebo group. Two were withdrawn from the active group, one because of severe angioneurotic oedema and the other because of vomiting and peripheral oedema. Both reactions subsided rapidly after drug withdrawal. Apart from these the side effects were stated to be only trivial, consisting chiefly of some dryness of the mouth and a tendency to constipation . 

Erythematous morbilliform, scarlatini-form, pruriginous and urticarial rashes have been observed (156 —164 ). Severe angioneurotic oedema developed in one patient on the second day of treatment with clopi-rac (156 ). 

Anaphylactic reactions of immediate type have been reported after intravenous injection of hydrocortisone sodium succinate (77, 99, 12 ). Skin tests were either negative or only positive to hydrocortisone or methylprednisolone proper. Cases of contact dermatitis and angioneurotic oedema are still being published (84 =). 

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