BackgroundPatients with obstructive sleep apnea-hypopnea syndrome (OSAHS) present with a variety of sleep-related symptoms. In polysomnography, sleep architecture is almost always abnormal, but it is not known which of the sleep-stage abnormalities are related to symptoms. Finding key sleep-stage abnormality that cause symptoms may be of therapeutic importance to alleviate symptoms. So far the mainstay of treatment is continuous positive airway pressure (CPAP)/bi-level positive airway pressure (BIPAP) therapy, but many patients are non-compliant to it. Correcting the sleep-stage abnormality that cause symptoms by pharmacotherapy may become an important adjunct to CPAP/BIPAP therapy.MethodsA cross-sectional study. Adult subjects who attended a sleep laboratory for diagnostic polysomnography for a period of 1 month were recruited consecutively. OSAHS was diagnosed using American Academy of Sleep Medicine criteria. Subjects filled a questionnaire for symptoms prior to polysomnography.ResultsThirty subjects, of whom 83.3% were obese, met diagnostic criteria, with males constituting 46.7% and females constituting 53%. Mean age was 53.40±11.60 years. Sleep architecture comprised N1 19.50±19.00%, N2 53.93±13.39%, N3 3.90±19.50%, and rapid eye movement 8.92±6.21%. Excessive fatigue or sleepiness, waking up tired, falling asleep during the day, trouble paying attention, snoring and insomnia were significantly related to decreased N3 sleep.ConclusionsMost of the symptoms in OSAHS in adults are related to decreased stage N3 sleep. If confirmed by larger controlled studies, correcting N3 sleep deficiency by pharmacotherapy may become an important adjunct to CPAP/BIPAP therapy to alleviate symptoms.

Clozapine is the preferred antipsychotic used for the treatment of resistant schizophrenia with suicidal ideation. The drug is started at a low dose and gradually increased to a target dose of 300–450 mg/day. It is well known to cause agranulocytosis and neutropenia. Several cases of fatal sepsis have been reported in neutropenic patients and emphasis is placed on monitoring for agranulocytosis; however, clozapine also causes intestinal hypomotility and constipation, which if unrecognized can lead to intestinal obstruction, bowel necrosis, and intra-abdominal sepsis. Reduced behavioral pain reactivity in schizophrenics may alter the ability to express pain, potentially leading to a delay in the presentation for medical attention. We report a case of fatal intra-abdominal sepsis secondary to an unrecognized case of clozapine-related constipation.

INTRODUCTION: Cannabis is the most commonly used recreational drug in the United States. Its abuse has been associated with Coronary thrombosis, Myocardial Infraction (MI), Ischemic stroke and central retinal vein thrombosis. We report a case of Sub-massive Pulmonary Embolism (PE) in a young male following heavy cannabis smoking. CASE PRESENTATION: 35-year-old Male with history of Schizophrenia presented to ER with worsening pleuritic chest pain, SOB and pain in the right leg for few days. Other review of systems was negative. He was incarcerated for last 16 months and was released 2 weeks prior to presentation. He was smoking cannabis heavily since his release. Physical examination was unremarkable except for tachycardia and initial labs showed troponin 0.16, BNP 419 and respiratory alkalosis. Urine toxicology was positive for cannabinoids. EKG revealed sinus tachycardia with T wave inversion in lateral leads. Chest X-Ray was unremarkable. CT chest revealed multiple large bilateral emboli and Echo showed right heart strain with moderate pulmonary hypertension. In next 24 hours he was hemodynamically unstable in respiratory distress requiring 10 Litre oxygen. He underwent catheter directed thrombolysis and was symptomatically better.the following day. Right pulmonary artery pressure decreased from 68/26 to 34/13. Duplex of leg veins showed a thrombus in right popliteal vein. Patient had no obvious risk factors for VTE. All workup for hypercoagulability was negative. DISCUSSION: Cannabis abuse has been associated with MI, Ischemic stroke, and Central retinal vein thrombosis in young patients. It is also known to trigger thrombosis in women using oral contraceptive pills. Cannabis induced VTE has not been reported except one case of PE in a young male. The exact mechanism by which cannabis induces hypercoagulability and thrombosis is still not well known. Some studies have reported that Cannabinoids, the active component of cannabis causes endothelial cell disruption leading to vascular thrombosis. In our case, cannabis in association with tobacco was the only risk factor, which we believe was the potential trigger that increased the risk of VTE. CONCLUSIONS: We illustrate a cause of VTE that mostly will be overlooked. Given the prevalence of cannabis use clinicians should consider it in their differential in a thrombotic event especially in young patients.

A 57-year-old woman presented with alcohol withdrawal symptoms, which later progressed to delirium tremens. During hospitalization, she developed respiratory distress with acute pulmonary edema. Electrocardiogram (ECG) showed diffuse ST elevation with elevated cardiac enzymes. Echocardiogram showed estimated ejection fraction of 20–25% with characteristic apical ballooning. After several days of supportive care, the patient showed significant clinical improvement with normalization of ECG, cardiac enzymes, and echocardiographic findings. Coronary angiogram revealed no coronary abnormalities. Although Takotsubo cardiomyopathy has been associated with diverse forms of physical or emotional stress, only a few cases have been described with delirium tremens in the medical literature.

We present a case of a middle-aged male who manifested with low-grade fever and lower back pain. MRI and bone scan of the spine were suggestive of vertebral osteomyelitis. Blood cultures were persistently positive for Enterococcus faecalis and echocardiogram revealed tricuspid valve endocarditis. There was no history of IV drug use and urine toxicology was negative. EKG showed Mobitz type II AV block and a transesophageal echocardiogram revealed no valve ring or septal abscesses. The heart block persisted despite antibiotic therapy and an epicardial pacemaker was placed. This is a rare presentation of high-grade AV block with tricuspid endocarditis in the absence of echocardiographic evidence of perivalvular extension of infection. Also, unique in this case is the finding of E. faecalis hematogenous vertebral osteomyelitis.