Neurological Sequelae After Acute Carbon Monoxide Poisoning.

Carbon monoxide poisoning (COP) is a common cause of death due to poisoning. After COP, a significant number of patients may develop a distinct type of neurological dysfunction called delayed neurological sequel (DNS). Recently, we came across a disaster of COP cases after a fire in a shared accommodation. The hostel was overcrowded and had a faulty air-conditioning/exhaust system. A total of five patients with loss of consciousness and shock were brought to us. They were diagnosed with acute COP based on their history of exposure to carbon monoxide (CO) and elevated carboxyhemoglobin levels in blood gas measurements. All patients were intubated and mechanically ventilated. Standard intensive care management was given to them, which included oxygenation, sedation, fluid resuscitation, and vasopressors. Their carboxyhemoglobin was rapidly reversed with normobaric oxygen therapy (NBO2). Three patients showed good response and neurological recovery after NBO2. Unfortunately, two patients developed DNS. DNS is a neuropsychological condition that may have cognitive, psychiatric, vestibulocochlear, motor, sensory, or diffuse demyelinating effects after COP. DNS is diagnosed in patients with a typical history of exposure to CO and a constellation of signs and symptoms. Neuroimaging, specifically magnetic resonance imaging of the brain with gadolinium contrast, is the method of choice for diagnosis. Treatment of DNS after COP begins with anticipation. All patients should receive appropriate oxygen therapy to bring down carboxyhemoglobin as soon as possible. Hyperbaric oxygen therapy (HBO2) for the treatment of COP and prevention of DNS is still debatable. In the available medical literature, there are conflicting recommendations regarding the use of HBO2 in COP/DNS. Moreover, apart from a lack of consensus, there is also a lack of clarity about optimum timing, duration, atmospheric pressure, and number of sessions of HBO2 in preventing DNS after COP. The development of DNS after COP is not directly responsible for mortality, but recovery sometimes takes a long time, which can contribute to increased morbidity and costs of treatment.

Epidemiology and outcome of an acute kidney injuries in the polytrauma victims admitted at the apex trauma center in Dubai.

BACKGROUND: Polytrauma from road accidents is a common cause of hospital admissions and deaths, frequently leading to acute kidney injury (AKI) and impacting patient outcomes. METHODS: This retrospective, single-center study included polytrauma victims with an Injury Severity Score (ISS) >25 at a tertiary healthcare center in Dubai. RESULTS: The incidence of AKI in polytrauma victims is 30.5%, associated with higher Carlson comorbidity index (P=0.021) and ISS (P=0.001). Logistic regression shows a significant relationship between ISS and AKI (odds ratio [OR], 1.191; 95% confidence interval [CI], 1.150-1.233; P<0.05). The main causes of trauma-induced AKI are hemorrhagic shock (P=0.001), need for massive transfusion (P<0.001), rhabdomyolysis (P=0.001), and abdominal compartment syndrome (ACS; P<0.001). On multivariate logistic regression AKI can be predicated by higher ISS (OR, 1.08; 95% CI, 1.00-1.17; P=0.05) and low mixed venous oxygen saturation (OR, 1.13; 95% CI, 1.05-1.22; P<0.001). The development of AKI after polytrauma increases length of stay (LOS)-hospital (P=0.006), LOS-intensive care unit (ICU; P=0.003), need for mechanical ventilation (MV) (P<0.001), ventilator days (P=0.001), and mortality (P<0.001). CONCLUSIONS: After polytrauma, the occurrence of AKI leads to prolonged hospital and ICU stays, increased need for mechanical ventilation, more ventilator days, and a higher mortality rate. AKI could significantly impact their prognosis.

What should an intensivist know about pneumocephalus and tension pneumocephalus?

Collection of air in the cranial cavity is called pneumocephalus. Although simple pneumocephalus is a benign condition, accompanying increased intracranial pressure can produce a life-threatening condition comparable to tension pneumothorax, which is termed tension pneumocephalus. We report a case of tension pneumocephalus after drainage of a cerebrospinal fluid hygroma. The tension pneumocephalus was treated with decompression craniotomy, but the patient later died due to the complications related to critical care. Traumatic brain injury and neurosurgical intervention are the most common causes of pneumocephalus. Pneumocephalus and tension pneumocephalus are neurosurgical emergencies, and anesthetics and intensive care management like the use of nitrous oxide during anesthesia and positive pressure ventilation have important implications in their development and progress. Clinically, patients can present with various nonspecific neurological manifestations that are indistinguishable from a those of a primary neurological condition. If the diagnosis is questionable, patients should be investigated using computed tomography of the brain. Immediate neurosurgical consultation with decompression is the treatment of choice.

Paget-Schroetter syndrome: An unfamiliar cause of upper-limb deep venous thrombosis.

Paget-Schroetter syndrome (PSS), which is also called "effort thrombosis," is a venous variant of thoracic outlet syndrome. We report a rare case of upper-limb deep venous thrombosis (ULDVT) in a young patient who was later diagnosed as PSS. PSS is a rare cause of ULDVT, and it is usually seen in young adults who are involved in strenuous physical activity. PSS is either due to anatomical abnormality of the thoracic outlet or due to repeated microtrauma to the endothelium of the subclavian/axillary vein. Clinically, the patient usually presents with signs and symptoms of ULDVT. Noninvasive Doppler ultrasonography is the initial investigation of choice, but computerized tomography and digital subtraction angiography are the gold standards for diagnosis. Treatment consists of therapeutic anticoagulation, catheter-directed thrombolysis, first rib resection, and postoperative oral anticoagulation. Although the PSS less likely causes pulmonary embolism, it can contribute to postthrombotic syndrome. PSS is a rare and distinct clinical entity, and most emergency care or primary care physicians are unaware of this condition. PSS requires rapid diagnosis, timely thrombolysis, and prompt referral to a vascular and thoracic surgeon.

Alveolar hemorrhage in a case of fat embolism syndrome: A case report with short systemic review.

Fat embolism and fat embolism syndrome (FES) are well-known complications of long bone fracture and surgery involving manipulation of skeletal elements. Many non-traumatic causes of FES have been suggested but they constitute only a small portion. FES presents with classical symptoms of petechiae, hypoxemia, central nervous system symptoms along with other features such as tachycardia and pyrexia. Diagnosis of FES relies on clinical judgment rather than objective findings such as emboli present in the retinal vessels on fundoscopy, fat globules present in urine and sputum, a sudden inexplicable drop in hematocrit or platelet values, increasing erythrocyte sedimentation rate.