Acne fulminans (also known as "acute febrile ulcerative acne": 686 ) is a severe form of the skin disease, acne, which can occur after unsuccessful treatment for another form of acne, acne conglobata. The condition is thought to be an immunologically induced disease in which elevated level of testosterone causes a rise in sebum and population of Cutibacterium acnes bacteria. The increase in the amount of C acnes or related antigens may trigger the immunologic reaction in some individuals and lead to an occurrence of acne fulminans. In addition to testosterone, isotretinoin may also precipitate acne fulminans, possibly related to highly increased levels of C acnes antigens in the patients immune system. Acne fulminans is a rare disease. Over the past several years, fewer cases of this disease have occurred, possibly because of earlier and better treatment of acne. Approximately 100 patients with acne fulminans have been described. Signs and symptoms
Acne fulminans begins as pain and inflammation in the joints. It eventually progresses into a swelling of the lymph nodes located at the base of the neck, causing inflexibility in the neck within weeks after the nodes swell. This swelling will eventually decrease, but this decrease will be accompanied by an increased inflammation and swelling of the joints, as well as a complete loss of appetite, though these symptoms are often ignored. After some time, the disease will cause an extreme loss of weight and atrophy of the muscles, leading to the decline of physical abilities.
Atrioventricular reentrant tachycardia (AVRT), or atrioventricular reciprocating tachycardia, is a type of abnormal fast heart rhythm and is classified as a type of supraventricular tachycardia (SVT). AVRT is most commonly associated with Wolff–Parkinson–White syndrome, but is also seen in permanent junctional reentrant tachycardia (PJRT). In AVRT, an accessory pathway allows electrical signals from the hearts ventricles to enter the atria and cause earlier than normal contraction, which leads to repeated stimulation of the atrioventricular node. Signs and symptoms
An episode of SVT may present with palpitations, dizziness, shortness of breath, or losing consciousness (fainting). The electrocardiogram (ECG) would appear as a narrow-complex SVT. Between episodes of tachycardia the affected person is likely to be asymptomatic; however, the ECG would demonstrate the classic delta wave in Wolff–Parkinson–White syndrome. Pathophysiology
Two distinct pathways are involved: the normal atrioventricular conduction system, and an accessory pathway. During AVRT, the electrical signal passes in the normal manner from the AV node into the ventricles. Then, the electrical impulse pathologically passes back into the atria via the accessory pathway, causing atrial contraction, and returns to the AV node to complete the reentrant circuit (see figure). Once initiated, the cycle may continue causing the heart to beat faster than usual.Initiation of AVRT may be through a premature impulse of atrial, junctional, or ventricular origin. Treatment
Acute management is as for SVT in general. The aim is to interrupt the circuit. In the shocked patient, DC cardioversion may be necessary. In the absence of shock, inhibition at the AV node is attempted.