The present study was designed to determine whether hyperoxia would lower the hypocapnic apneic threshold (AT) during non-rapid eye movement (NREM) sleep. Nasal noninvasive mechanical ventilation was used to induce hypocapnia and subsequent central apnea in healthy subjects during stable NREM sleep. Mechanical ventilation trials were conducted under normoxic (room air) and hyperoxic conditions (inspired PO(2) > 250 Torr) in a random order. The CO(2) reserve was defined as the minimal change in end-tidal PCO(2) (PET(CO(2))) between eupnea and hypocapnic central apnea. The PET(CO(2)) of the apnea closest to eupnea was designated as the AT. The hypocapnic ventilatory response was calculated as the change in ventilation below eupnea for a given change in PET(CO(2)). In nine participants, compared with room air, exposure to hyperoxia was associated with a significant decrease in eupneic PET(CO(2)) (37.5 ± 0.6 vs. 41.1 ± 0.6 Torr, P = 0.001), widening of the CO(2) reserve (-3.8 ± 0.8 vs. -2.0 ± 0.3 Torr, P = 0.03), and a subsequent decline in AT (33.3 ± 1.2 vs. 39.0 ± 0.7 Torr; P = 001). The hypocapnic ventilatory response was also decreased with hyperoxia. In conclusion, 1) hyperoxia was associated with a decreased AT and an increase in the magnitude of hypocapnia required for the development of central apnea. 2) Thus hyperoxia may mitigate the effects of hypocapnia on ventilatory motor output by lowering the hypocapnic ventilatory response and lowering the resting eupneic PET(CO(2)), thereby decreasing plant gain.
Background: There are no standard therapies for the management of central sleep apnea (CSA). Either positive pressure therapy (PAP) or supplemental oxygen (O 2 ) may stabilize respiration in CSA by reducing ventilatory chemoresponsiveness. Additionally, increasing opioid use and the presence of comorbid conditions in US veterans necessitates investigations into alternative titration protocols to treat CSA. The goal was to report on the effectiveness of titration with PAP, used alone or in conjunction with O 2 , for the management of CSA associated with varying comorbidities and opioid use. Methods: This was a retrospective chart review over 3 years, performed at a VA sleep disorders center. The effects of CPAP, CPAP+O 2 , and BPAP+O 2 , used in a step-wise titration protocol, on consecutive patients diagnosed with CSA were studied. Results: CSA was diagnosed in 162 patients. The protocol was effective in eliminating CSA (CAI ≤ 5/h) in 84% of patients. CPAP was effective in 48%, while CPAP+O 2 combination was effective in an additional 25%, and BPAP+O 2 in 11%. The remaining 16% were non-responders. Forty-seven patients (29%) were on prescribed opioid therapy for chronic pain, in whom CPAP, CPAP+O 2 , or BPAP+O 2 eliminated CSA in 54%, 28%, and 10% cases,, respectively. CPAP, CPAP+O 2 , and BPAP+O 2 each produced signifi cant declines in the AHI, CAI, and arousal index, and an increase in the SpO 2 .Conclusion: The data demonstrate that using a titration protocol with CPAP and then PAP with O 2 effectively eliminates CSA in individuals with underlying comorbid conditions and prescription opioid use. Comparative studies with other therapeutic modalities are required. S C I E N T I F I C I N V E S T I G A T I O N ST he treatment of central sleep apnea (CSA) continues to lack a universally recognized standard of care.1 Variable etiologies of CSA and the presence of concomitant disorders infl uence the choice of therapy. Thus, therapeutic options have varied markedly from positive airway pressure (PAP) devices, including continuous positive airway pressure (CPAP), 2-6 bilevel positive airway pressure therapy (BPAP), 7-9 and adaptive servoventilation, [10][11][12][13]20 to supplemental O 2 , 14-17 carbon dioxide, 21,22 and/or pharmacologic agents. [23][24][25]29,30 The outcomes of therapy have also varied considerably, with limited evidence to establish the effectiveness of any therapy for CSA. [26][27][28][29]31,32 The majority of published literature has focused on the treatment of CSA secondary to congestive heart failure (CHF), [2][3][4][5][6][7][8][9][10][11][15][16][17][18][19][20][21][22][26][27][28][29] with very little data on patients with "primary" CSA 23,24 or CSA secondary to causes other than CHF. 33 In addition, there is very little data on the treatment of CSA related to opioid use and CSA that is concomitant with OSA. 13,35 The latter entities are of increasing importance in the US veteran population due to the increased use of prescription opioid drugs for chronic pain control and the risk for opioi...
Canagliflozin (Invokana) is a selective sodium glucose cotransporter-2 (SGLT-2) inhibitor that was first introduced in 2013 for the treatment of type 2 diabetes mellitus (DM). Though not FDA approved yet, its use in type 1 DM has been justified by the fact that its mechanism of action is independent of insulin secretion or action. However, some serious side effects, including severe anion gap metabolic acidosis and euglycemic diabetic ketoacidosis (DKA), have been reported. Prompt identification of the causal association and initiation of appropriate therapy should be instituted for this life threatening condition.
Four patients with pseudocyst of the spleen gave histories of abdominal trauma. In one patient the pseudocyst had ruptured, necessitating emergency splenectomy 34 years after the original injury. In a second patient the pseudocyst was discovered incidentally, and was managed by spleen-preserving excision; and the third and fourth presented with abdominal pain and had splenectomy and spleen-preserving surgery, respectively. All patients with conservatively treated splenic injury are at risk of developing a pseudocyst of the spleen, and the lesion can be detected by computed tomography or ultrasound. When there are no symptoms the natural history is unknown; but if surgery is necessary, splenectomy can sometimes be avoided.
IntroductionNon-typhoidal Salmonella (NTS) is mostly restricted to gastroenteritis; however, we report a case of Salmonella pericarditis complicated by tamponade and spontaneous ventricular wall rupture.Case presentationA 67-year-old male presents to the Emergency Department with complaints of fevers, chills and body aches. A chest radiograph displayed an infiltrate and an electrocardiogram suggested acute pericarditis. An echocardiogram revealed a small pericardial effusion without tamponade. Broad-spectrum antibiotics were initiated until Salmonella was discovered in blood cultures. The hospital course was complicated by sudden decompensation, and a repeat echocardiogram displayed a large effusion with constrictive physiology. During a pericardial window, the tissue was noted to have a thickened appearance with a complex effusion. The following day, the patient developed increased chest tube drainage, hypotension and acidosis, requiring an emergent sternotomy. The right ventricle was friable and had spontaneously ruptured. After ventricular repair and pericardiectomy, the tissue was sent for cultures and pathology. The specimen revealed Salmonella enteriditis. Treatment with ceftriaxone and ciprofloxacin was initiated. On postoperative day four, the patient was successfully extubated. Repeat blood cultures were negative.DiscussionIn our review of literature, only 19 cases of NTS pericarditis have been reported. Prior to our case, salmonellosis resulting in ventricular rupture has been reported once. Early diagnosis and treatment is crucial in minimizing morbidity and mortality. Clinical suspicion based on electrocardiogram and hemodynamic assessment is critical in suspecting pericardial effusion in a patient with nonspecific symptoms and Salmonella bacteremia. The key to recovery involves aggressive treatment, including pericardiectomy and antibiotic treatment.
Streptococcus gallolyticus subspecies (subsp.) gallolyticus (formerly bovis biotype I) bacteremia has been associated with colonic adenocarcinoma. The bovis species underwent reclassification in 2003. Subtypes of gallolyticus are associated with colonic malignancy but are less frequent, resulting in less awareness. A 71-year-old male admitted with worsening lower back pain and fevers. Initial vital signs and laboratory data were within normal limits. MRI revealed lumbosacral osteomyelitis and antibiotics were initiated. Blood cultures showed Streptococcus species, prompting a transesophageal echocardiogram (TEE) revealing vegetations on the mitral and aortic valves. The etiology for his endocarditis was unclear. A colonoscopy was suggested, but his clinical instability made such a procedure intolerable. Final cultures revealed Streptococcus gallolyticus subsp. pasteurianus (previously bovis biotype II). After antibiotic completion he underwent aortic grafting with valve replacements. Later, he was readmitted for Streptococcus bacteremia. After a negative TEE, colonoscopy revealed a 2.5 × 3 cm cecal tubulovillous adenoma with high-grade dysplasia suspicious for his origin of infection. Clinicians understand the link between Streptococcus gallolyticus subsp. gallolyticus (bovis type I) and malignancy, but the new speciation may be unfamiliar. There are no guidelines for managing S. gallolyticus subsp. pasteurianus bacteremia; therefore a colonoscopy should be considered when no source is identified.
Editor-We would like to highlight an infrequent but serious adverse effect of tramadol. We report a case of generalized tonic-clonic seizure associated with sympathetic nervous system hyperactivity, which included profuse diaphoresis, tachycardia (HR: 136 beats min 21), hypertension (BP: 160/110 mm Hg), and widespread erythema after the administration of tramadol. A healthy 49-yr-old male was admitted to hospital for management of a fractured humerus. The only medication the patient received was morphine 30 mg followed by oral tramadol 100 mg approximately 40 min before the grand mal seizure. Tramadol can precipitate seizures in epileptic patients 1-3 by lowering the seizure threshold. There have been several case reports of tramadol precipitating a seizure in non-epileptic patients. However, our patient had a more complicated seizure presentation, which included generalized erythema, and profuse sustained diaphoresis. Tramadol increases cerebral serotonin activity by partial inhibition of its uptake, particularly when it is given in combination with other drugs including morphine. This increased serotonin activity can produce serotonin syndrome which is characterized by disorders in cognitive-behavioural, neuromuscular, and autonomic function. 4 5 To qualify for the diagnosis, it has been suggested that a patient should have at least one or two manifestations from each of these functional categories. There is no formal test for the diagnosis of serotonin syndrome. The onset of clinical effects is relatively rapid (minutes to a few hours). Management is discontinuation of the causative agents with supportive treatment and the clinical symptoms and signs usually resolve within 24 h. Hyperthermia should be treated with active cooling. Rigidity, seizures, and agitation should be treated with benzodiazepines. Severe symptoms have been treated successfully with cyproheptadine-a 5-HT2 antagonist.
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