William A. Marinelli

Intensive care unit drug use and subsequent quality of life in acute lung injury patients

ObjectiveTo examine the relationship between the use of sedative and neuromuscular blocking agents during a patient’s intensive care unit (ICU) stay and subsequent measures of health-related quality of life. DesignCross-sectional mail survey and retrospective medical record abstraction of a prospectively identified cohort of lung injury patients. SettingICUs in three teaching hospitals in a major metropolitan area. PatientsPatients with acute lung injury (n = 24). InterventionsNone—observational study. Measurements and Main ResultsPatients’ charts were reviewed for those patients returning postdischarge quality-of-life questionnaires. Duration, daily dose, and route of administration for sedatives and neuromuscular blocking agents were abstracted from ICU flow sheets. Relationships among ICU variables (days of sedation, days of neuromuscular blockade, and severity of illness as measured by Acute Physiology and Chronic Health Evaluation III score) and outcomes (symptoms of depression and symptoms of posttraumatic stress disorder) were assessed. Depressive symptoms at follow-up were correlated with days of sedation (p = .007), but not with days of neuromuscular blockade or initial severity of illness. The composite posttraumatic stress disorder symptom impact score was correlated with days of sedation (p = .006) and days of neuromuscular blockade (p = .035), but not with initial severity of illness. There were no significant differences between the frequency of patients reporting a specific posttraumatic stress disorder symptom in the high sedation group and the low sedation group, and there were no significant differences in specific posttraumatic stress disorder symptoms between the group that had received neuromuscular blockade and those who had not. ConclusionsThe use of sedatives and neuromuscular blocking agents in the ICU is positively associated with subsequent measures of depression and posttraumatic stress disorder symptoms 6–41 months after ICU treatment for acute lung injury.

Acute lung injury. Pathogenesis of intraalveolar fibrosis.

In patients dying with acute lung injury, interstitial mesenchymal cells migrate into the airspace where they replicate and deposit connective tissue. We therefore hypothesized that peptides capable of promoting mesenchymal cell migration and replication would be present in the alveolar airspace. To examine this hypothesis, patients with severe acute diffuse lung injury (n = 26) underwent bronchoalveolar lavage. Acutely ill patients without lung injury served as controls (n = 12). Recovered effluent was examined for mesenchymal cell growth-promoting and migration-promoting activity. Lavage cell supernates from both patients and controls were devoid of bioactivity. However, substantial growth-promoting and migration-promoting activity was present in lavage fluid from nearly every patient, whereas little or none was present in fluid from controls. Characterization of the bioactivity indicated a significant proportion consisted of three peptides related to PDGF: (a) a 14-kD peptide that shared with PDGF several biophysical, biochemical, receptor-binding, and antigenic properties; (b) a 29-kD peptide that appeared identical to PDGF of platelet origin; and (c) a 38-kD peptide that was biophysically and antigenically similar to PDGF. These data indicate that peptide moieties are present in the airspace of patients after acute lung injury that can signal mesenchymal cell migration and replication.

Neuromuscular disorders in the intensive care unit

Neuromuscular disorders encountered in the ICU can be categorized as muscular diseases that lead to ICU admission and those that are acquired in the ICU. This article discusses three neuromuscular disorders can lead to ICU admission and have a putative immune-mediated pathogenesis: the Guillian-Barré syndrome, myasthenia gravis, and dermatomyositis/polymyositis. It also reviews critical care polyneuropathy and ICU acquired myopathy, two disorders that, alone or in combination, are responsible for nearly all cases of severe ICU acquired muscle weakness.

An unusual cause of cardiopulmonary arrest.

A 43-year-old man arrived at our emergency department (ED) entrance in a private vehicle. The patient’s family members summoned help, reporting that the patient had suddenly lost consciousness and become cyanotic. The patient’s sister expressed concern that the patient may have used intravenous heroin. There was no preceding trauma. The patient’s medical history was significant for type II diabetes mellitus and intravenous drug abuse. The primary survey revealed an apneic patient without palpable pulses. Cardiopulmonary resuscitation was immediately initiated, and the patient was moved to the ED critical care area. Return of spontaneous circulation was rapidly achieved. Intravenous access was established and 4 mg of intravenous naloxone was administered without response. The patient was orotracheally intubated without the need for sedation or paralysis. Upon secondary survey, the patient’s eyes were open, and he was clenching his teeth on the endotracheal tube. However, he had no movement of his extremities in response to commands or noxious stimuli (GCS 6T). There were track marks on his arms consistent with IVDU. The remainder of his examination was unremarkable. Initial laboratory studies were unrevealing. The ECG showed a sinus tachycardia. Central venous access was obtained, and post-cardiac arrest cooling was initiated. He was given ketamine and vecuronium just prior to being transferred to the medical intensive care unit (MICU). Immediately following admission to the MICU, sedatives and paralytics were briefly held to facilitate re-examination. Upon re-examination, the patient was noted to be tracking the examiner with his eyes. He responded to questions with blinking, and he had full extra ocular movements but no other motor movement to command. His reflexes were brisk throughout, and he exhibited weak triple flexion of his bilateral lower extremities. Based upon his examination, a cervical collar was immediately placed, and neurosurgery was emergently consulted as the patient was transported for radiographic imaging of his cervical spine (c-spine). Computed tomography (CT) of the patient’s c-spine revealed a comminuted odontoid fracture with complete atlantoaxial (C1-C2) dislocation as well as vertebral erosions, severe ligamentous injury, and paravertebral fluid collections (Fig. 1). The differential included infectious, other inflammatory, and traumatic etiologies. A halo traction device was placed for stabilization, and the patient was started on ceftriaxone and vancomycin empirically. Bacterial cultures from transoral aspiration of the fluid collections grew methicillin-resistant Staphylococcus aureus (MRSA). The patient subsequently underwent occiput-to-C4 fusion, and completed a course of longterm IV antibiotic therapy. On follow-up examinations, his executive function remained intact, but his motor examination remained poor with complete quadriplegia and ventilator dependence. Cardiopulmonary arrest resulting from cervical spinal cord injury occurs due to paralysis of the respiratory muscles or disruption of the autonomic nervous system resulting in cardiovascular collapse (i.e. neurogenic shock & Kenneth W. Dodd kdoddmd@gmail.com