Delayed pulmonary dysfunction in head-injured patients

Abstract

Intracranial pressure (ICP), cardiopulmonary function, and the degree of neurological dysfunction were measured in 13 patients with serious head injury to determine the relationship of these indices to the development of delayed pulmonary dysfunction. All patients had serious isolated head injury with Glasgow Coma Scale scores of 7 or less 6 hours after injury and elevated ICP at the time of admission to the protocol. Three patients developed arterial pO2 of less than or equal to 80 torr despite the initiation of elevated inspired oxygen fraction (FIO2 greater than or equal to 0.5) and positive end expiratory pressure (greater than or equal to 5 cm H2O. One of these three patients had a decline in neurological function, quantified by the Albany Head-Injury Watch Sheet, associated with hypoxemia. The only patients who developed intrapulmonary shunt fractions of more than 15% were five patients who had increased pulmonary vascular resistance (PVR) and elevated or increasing cardiac index, suggesting persistent perfusion to areas of the lung which normally are hypoperfused due to hypoxic pulmonary vasoconstriction. This mismatching of the distribution of ventilation and perfusion was confirmed using the multiple inert gas elimination technique in two patients with an increased shunt fraction. Unperfused gas exchange units were also found to be present, as confirmed by an abnormal multiple inert gas elimination techniques, high PVR and dead space/tidal volume ratio (VD/VT), and low extravascular lung water. Abnormalities of ICP and cerebral perfusion pressure could not be correlated with changes in any of the cardiopulmonary functions studied.

Acidentes de motocicleta no Município de São Paulo, SP, Brasil: 2. análise da mortalidade

“…O primeiro está demonstrado tanto em animais como em seres humanos, enquanto que a insuficiên-cia respiratória tardia ainda continua pouco esclarecida 26 .…”

“…Segundo Popp e col. 26 , grande nú-mero de pacientes com edema pulmonar fulminante, após traumatismo crânio-encefálico, sustenta a existência de edema pulmonar neurogênico como uma entidade distinta. Achados de pacientes que morreram imediatamente após trauma craniano mostraram que o edema pulmonar, a congestão e a hemorragia intraalveolar sugerem a origem neurogênica, desde que os outros fatores como o desequilíbrio hídrico, a embolia gordurosa ou a microembolização não poderiam ter ocorrido nesse período de tempo entre o acidente e a morte.…”

“…Como estas alterações podem ser decorrentes primariamente da aspiração endotraqueal, pneumonia, pneumotórax ou contusão pulmonar e secundários à lesão pulmonar como falência cardíaca, septicemia, desequilíbrio hídrico ou embolia gordurosa, explica-se a alta freqüência de complicações pulmonares nesses pacientes 26 .…”

Aggressive Physiologic Monitoring of Pediatric Head Trauma Patients with Elevated Intracranial Pressure

“…This increased PVR could possibly be due to raised ICP causing greater sympathetic discharge that produces severe pulmonary vascular constriction without producing marked systemic hypertension or left ventricular failure [24,29,30], PVR did decrease to baseline values during the course of therapy.…”

“…Effects of trauma and pentobarbital coma can lead to atelectasis. That and ag gressive fluid predispose formation of pulmonary ede ma, decreased mucociliary clearance, infection, and subsequent increased pulmonary vasoconstriction [24,29,30].…”