Position of draining venous cannula in extracorporeal membrane oxygenation for respiratory and respiratory/circulatory support in adult patients.

Extracorporeal membrane oxygenation (ECMO) is used in critically ill patients with severe pulmonary and/or cardiac failure. Blood is drained from the venous system and pumped through a membrane oxygenator where it is oxygenated. For pulmonary support, the blood is returned to the patient via a vein (veno-venous ECMO) and for pulmonary/circulatory support it is returned via an artery (veno-arterial ECMO).Veno-venous ECMO can be performed either with a single dual-lumen cannula or with two separate single-lumen cannulas. If the latter is chosen, flow direction can either be from the inferior caval vein (IVC) to the right atrium or the opposite. Earlier research has shown that drainage from the IVC yields less recirculation and therefore the IVC to right atrium route has become the standard in most centers for veno-venous ECMO with two cannulas. However, recent research has shown that recirculation can be minimized using a multistage draining cannula in the optimal position inserted via the right internal jugular vein and with blood return to the femoral vein. The clinical results with this route are excellent.In veno-arterial ECMO the most common site for blood infusion is the femoral artery. If venous blood is drained from the IVC, the patient is at risk of developing a dual circulation (Harlequin syndrome, North-South syndrome, differential oxygenation) meaning a poor oxygenation of the upper part of the body, while the lower part has excellent oxygenation. By instead draining from the superior caval vein (SVC) via a multistage cannula inserted in the right internal jugular vein this risk is neutralized.In conclusion, the authors argue that draining blood from the SVC and right atrium via a multistage cannula inserted in the right internal jugular vein is equal or better than IVC drainage both in veno-venous two cannula ECMO and in veno-arterial ECMO with blood return to the femoral artery.

Acquired idiopathic generalized anhidrosis: case report.

We report a case of acquired idiopathic generalized anhidrosis (AIGA) in a 56-year-old white woman. Acquired idiopathic generalized anhidrosis is an exceedingly rare group of heterogeneous disorders that has been almost exclusively reported in young Japanese males. Our case is unique in that AlGA may be underrecognized in this patient population.

Drug-induced hyperhidrosis and hypohidrosis: incidence, prevention and management.

The human sweating response is subject to the influence of diverse classes of drugs. Some act centrally at the hypothalamus or at spinal thermoregulatory centres, while others act at sympathetic ganglia or at the eccrine-neuroeffector junction. Pharmacological disturbances of sweating have broad clinical implications. Drugs that induce hyperhidrosis, or sweating in excess of that needed to maintain thermoregulation, can cause patient discomfort and embarrassment, and include cholinesterase inhibitors, selective serotonin reuptake inhibitors, opioids and tricyclic antidepressants. Drugs that induce hypohidrosis, or deficient sweating, can increase the risk of heat exhaustion or heat stroke and include antimuscarinic anticholinergic agents, carbonic anhydrase inhibitors and tricyclic antidepressants. As acetylcholine is the principal neuroeccrine mediator, anhidrosis is one of the clinical hallmarks by which acute anticholinergic toxicity may be recognized. The symptom of dry mouth often accompanies the less apparent symptom of hypohidrosis because the muscarinic M(3) acetylcholine receptor type predominates at both sweat and salivary glands. Management options include dose reduction, drug substitution or discontinuation. When compelling medical indications require continuation of a drug causing hyperhidrosis, the addition of a pharmacological agent to suppress sweating can help to reduce symptoms. When hypohidrotic drugs must be continued, deficient sweating can be managed by avoiding situations of heat stress and cooling the skin with externally applied water. The availability of clinical tests for the assessment of sudomotor dysfunction in neurological disease has enhanced recognition of the complex effects of drugs on sweating. Advances in the understanding of drug-induced anhidrosis have also enlarged the therapeutic repertoire of effective treatments for hyperhidrosis.

Predictive value of acetylcholine stimulation testing for oligohidrosis caused by zonisamide.

We studied 16 patients for whom zonisamide was newly prescribed. Acetylcholine stimulation testing was performed about 1 month after zonisamide was initiated. Oligohidrosis occurred in none of the four with a normal response and in four of the 12 with a decreased response. Acetylcholine stimulation testing predicted oligohidrosis with a sensitivity of 1 and a false-positive rate of 0.67. The acetylcholine stimulation test was sensitive in detecting oligohidrosis caused by zonisamide, although the false-positive rate was high.