Association of pulmonary hypertension with survival and neurologic outcomes in adults with in-hospital cardiac arrest.

BACKGROUND: Pulmonary hypertension (PH) has been associated with poor survival in multiple cardiopulmonary conditions, however its association with outcomes in cardiac arrest remains unknown. We aimed to evaluate the association of PH with survival and neurologic outcomes in adults with in-hospital cardiac arrest (IHCA). METHODS: The study population included adults with IHCA undergoing resuscitation at an academic tertiary-care medical center from 2011 to 2019. Patients were classified based upon the presence versus absence of PH, defined as a pulmonary artery systolic pressure >35 mmHg on pre-arrest echocardiogram. Survival to discharge and favorable neurological outcome (defined as a Glasgow Outcome Score of 4-5) served as the primary and secondary outcomes of interest respectively. RESULTS: Of the 371 patients studied, 203 (54.7%) had PH while 168 (45.3%) did not. Patients with PH had higher Charlson Comorbidity Score with higher rates of multiple baseline comorbidities. They also had worse multi-chamber enlargement, left ventricular diastolic dysfunction, right ventricular systolic dysfunction, and valvular heart disease compared to non-PH patients. Rates of survival to discharge (11.5% vs 10.9%, p = 0.881) and favorable neurologic outcome (8.0% vs 6.2%, p = 0.550) were similar in PH and non-PH patients respectively. In multivariable analysis, PH was not associated with survival to discharge (OR 1.23, 95%CI 0.57-2.65) or favorable neurologic outcome (OR 1.69, 95%CI 0.64-4.45). CONCLUSIONS: In this contemporary registry of adults with IHCA, while PH was associated with a higher risk patient profile, it was not associated with survival or neurologic outcomes in this population.

Cocaine-induced rhabdomyolysis and compartment syndrome.

A man in his 30s with a history of cocaine and intranasal heroin use presented to the emergency department with severe leg pain and weakness. Physical examination findings were significant for tachycardia, absence of dorsalis pedis pulses, tense and painful calf muscles along with absence of plantar reflexes in bilateral lower extremities. Laboratory investigations were significant for positive urinary drug screen for cocaine, severe rhabdomyolysis and acute kidney injury. Given the absence of dorsalis pedis pulses in bilateral lower extremities and radiological evidence of oedematous changes in calf muscles with perimuscular oedema, a diagnosis of compartment syndrome was made. He was treated with bilateral lower extremity four-compartment fasciotomies and haemodialysis for acute kidney injury. Rhabdomyolysis has been attributed to cocaine use; however, compartment syndrome is a very rare complication, especially in the absence of trauma or prolonged immobilisation.

Face Mask Leak Determines Aerosol Delivery in Noninvasive Ventilation.

BACKGROUND: Aerosol transport during noninvasive ventilation follows the flow of pressurized gas through the noninvasive ventilation circuit, vented via leak port and face mask, and inhaled by the patient. Recommendations for nebulizer placement are based on in vitro models that have focused primarily on aerosol losses via the leak port; face mask leaks have been avoided. This study tested aerosol delivery in the setting of controlled face mask leak. METHODS: Three nebulizer technologies were studied on a bench model using a lung simulator with a face mask placed onto a manikin head. Radiolabeled aerosol delivery (ie, inhaled mass) was determined by mass balance using filters and a gamma camera that tested the effects of nebulizer location and face mask leak. Low (15-20 L/min) and high (55-60 L/min) mask leaks were used to mimic realistic clinical conditions. RESULTS: Inhaled mass (% nebulizer charge) was a function of nebulizer technology (with the nebulizer at ventilator outlet position: Aerogen 22.8%, InspiRx 11.1%, and Hudson 8.1%; P = .001). The location of the nebulizer before or after the leak port was not important (P = 0.13 at low leak and P = 0.38 at high leak). Aerosol delivery was minimal with high mask leak (inhaled mass 1.5-7.0%). Aerosol losses at the leak port at low mask leak were 28-36% versus 9-24% at high mask leak. Aerosol losses via the mask leak were 16-20% at low mask leak versus 46-72% at high mask leak. Furthermore, high face mask leak led to significant deposition on the mask and face (eg, up to 50% of the nebulizer charge with the Aerogen mask). CONCLUSIONS: During noninvasive ventilation, nebulizer placement at the ventilator outlet, which is a more practical position, is effective and minimizes deposition on face and mask. Aerosol therapy should be avoided when there is high face mask leak.

Pulmonary hypertension in chronic hemolytic anemias: Pathophysiology and treatment.

Pulmonary hypertension has emerged as a major cause of morbidity and mortality in patients with hemoglobinopathies and chronic hemolytic anemias. These hematological diseases include - but are not limited to - sickle cell disease (SCD), thalassemia, paroxysmal nocturnal hematuria, and hereditary spherocytosis. Although most studies have been based on the use of echocardiography as a screening tool for pulmonary hypertension as opposed to the gold standard of right heart catheterization for definitive diagnosis, the association between chronic hemolytic anemia and pulmonary hypertension is evident. Studies have shown that patients with SCD and a tricuspid regurgitant velocity (TRV) ≥ 2.5 m/sec are at increased risk of pulmonary hypertension and are at increased mortality risk. Additional markers of risk of pulmonary hypertension and increased mortality include a pro-BNP >160 pg/mL combined with a 6-min walk distance of <333 m. There is currently a lack of concrete data to support the use of targeted oral pulmonary arterial hypertension therapy in chronic hemolytic anemia. As a result, management is generally targeted towards medical optimization of the underlying anemia. This literature review aims to discuss the pathophysiology, diagnostic and prognostic tools, recent studies and current protocols that are essential in guiding management of pulmonary hypertension in chronic hemolytic anemias.

A 47-Year-Old Man With Recurrent Unilateral Pleural Effusion.

CASE PRESENTATION: A 47-year-old man with a medical history of hypertension, diabetes, hyperlipidemia, and OSA presented with a 7- to 10-day history of progressively worsening dyspnea on exertion, with a walking distance of 60 feet. He had bilateral lower-extremity swelling and was prescribed furosemide without clinical improvement. At baseline, he used three pillows for sleeping. The patient was noncompliant with his CPAP treatment. He had no smoking history and was retired from working in technology sales. On review of systems, he denied cough, chest pain, hemoptysis, fevers, chills, or weight loss.

Transforming growth factor-beta1 impairs neuropathic pain through pleiotropic effects.

BACKGROUND: Understanding the underlying mechanisms of neuropathic pain caused by damage to the peripheral nervous system remains challenging and could lead to significantly improved therapies. Disturbance of homeostasis not only occurs at the site of injury but also extends to the spinal cord and brain involving various types of cells. Emerging data implicate neuroimmune interaction in the initiation and maintenance of chronic pain hypersensitivity. RESULTS: In this study, we sought to investigate the effects of TGF-beta1, a potent anti-inflammatory cytokine, in alleviating nerve injury-induced neuropathic pain in rats. By using a well established neuropathic pain animal model (partial ligation of the sciatic nerve), we demonstrated that intrathecal infusion of recombinant TGF-beta1 significantly attenuated nerve injury-induced neuropathic pain. TGF-beta1 treatment not only prevents development of neuropathic pain following nerve injury, but also reverses previously established neuropathic pain conditions. The biological outcomes of TGF-beta1 in this context are attributed to its pleiotropic effects. It inhibits peripheral nerve injury-induced spinal microgliosis, spinal microglial and astrocytic activation, and exhibits a powerful neuroprotective effect by preventing the induction of ATF3+ neurons following nerve ligation, consequently reducing the expression of chemokine MCP-1 in damaged neurons. TGF-beta1 treatment also suppresses nerve injury-induced inflammatory response in the spinal cord, as revealed by a reduction in cytokine expression. CONCLUSION: Our findings revealed that TGF-beta1 is effective in the treatment of neuropathic by targeting both neurons and glial cells. We suggest that therapeutic agents such as TGF-beta1 having multipotent effects on different types of cells could work in synergy to regain homeostasis in local spinal cord microenvironments, therefore contributing to attenuate neuropathic pain.