The act of breathing depends on coordinated activity of the respiratory muscles to generate subatmospheric pressure. This action is compromised by disease states affecting anatomical sites ranging from the cerebral cortex to the alveolar sac. Weakness of the respiratory muscles can dominate the clinical manifestations in the later stages of several primary neurologic and neuromuscular disorders in a manner unique to each disease state. Structural abnormalities of the thoracic cage, such as scoliosis or flail chest, interfere with the action of the respiratory muscles-again in a manner unique to each disease state. The hyperinflation that accompanies diseases of the airways interferes with the ability of the respiratory muscles to generate subatmospheric pressure and it increases the load on the respiratory muscles. Impaired respiratory muscle function is the most severe consequence of several newly described syndromes affecting critically ill patients. Research on the respiratory muscles embraces techniques of molecular biology, integrative physiology, and controlled clinical trials. A detailed understanding of disease states affecting the respiratory muscles is necessary for every physician who practices pulmonary medicine or critical care medicine.

Disorders of the Respiratory Muscles

Significant advances in vascular disease medical intervention since large randomized trials for asymptomatic severe carotid stenosis were conducted (1983–2003) have prompted doubt over current expectations of a surgical benefit. In this systematic review and analysis of published data it was found that rates of ipsilateral and any-territory stroke (+/−TIA), with medical intervention alone, have fallen significantly since the mid-1980s, with recent estimates overlapping those of operated patients in randomized trials. However, current medical intervention alone was estimated at least 3 to 8 times more cost-effective. In conclusion, current vascular disease medical intervention alone is now best for stroke prevention associated with asymptomatic severe carotid stenosis given this new evidence, other cardiovascular benefits, and because high-risk patients who benefit from additional carotid surgery or angioplasty/stenting cannot be identified.

Medical (nonsurgical) intervention alone is now best for prevention of stroke associated with asymptomatic severe carotid stenosis: results of a systematic review and analysis.

The decision to treat a patient in the intensive care unit (ICU) with neuromuscular blocking agents (NMBAs) (for reasons other than the placement of an endotracheal tube) is a difficult one that is guided more commonly by individual practitioner preference than by standards based on evidence-based medicine. Commonly cited reasons for the use of NMBAs in the ICU are to facilitate mechanical ventilation or different modes of mechanical ventilation and to manage patients with head trauma or tetanus. Independent of the reasons for using NMBAs, we emphasize that all other modalities to improve the clinical situation must be tried, using NMBAs only as a last resort. In 1995, the American College of Critical Care Medicine (ACCM) of the Society of Critical Care Medicine (SCCM) published guidelines for the use of NMBAs in the ICU. The present document is the result of an attempt to reevaluate the literature that has appeared since the last guidelines were published and, based on that review, to update the recommendations for the use of NMBAs in the ICU. Appendix A summarizes our recommendations. Using methods previously described to evaluate the literature and grade the evidence (1), the task force reviewed the physiology of the neuromuscular receptor, the pharmacology of the NMBAs currently used in the ICU, the means to monitor the degree of blockade, the complications associated with NMBAs, and the economic factors to consider when choosing a drug.

/pdf/clinical-practice-guidelines-for-sustained-neuromuscular-2yi6vl70ek.pdf

Clinical practice guidelines for sustained neuromuscular blockade in the adult critically ill patient

Critical illness, more precisely defined as the systemic inflammatory response syndrome (SIRS), occurs in 20%-50% of patients who have been on mechanical ventilation for more than 1 week in an intensive care unit. Critical illness polyneuropathy (CIP) and myopathy (CIM), singly or in combination, occur commonly in these patients and present as limb weakness and difficulty in weaning from the ventilator. Critical illness myopathy can be subdivided into thick-filament (myosin) loss, cachectic myopathy, acute rhabdomyolysis, and acute necrotizing myopathy of intensive care. SIRS is the predominant underlying factor in CIP and is likely a factor in CIM even though the effects of neuromuscular blocking agents and steroids predominate in CIM. Identification and characterization of the polyneuropathy and myopathy depend upon neurological examination, electrophysiological studies, measurement of serum creatine kinase, and, if features suggest a myopathy, muscle biopsy. The information is valuable in deciding treatment and prognosis.

Neuromuscular manifestations of critical illness.

An acute myopathy of intensive care occurs in critically ill patients treated with intravenous corticosteroids and neuromuscular junction-blocking agents. The full clinicopathological spectrum is uncertain. We evaluated the clinical, electrodiagnostic, and histopathological features of 14 patients who developed acute myopathy of intensive care after organ transplantation or during treatment of severe pulmonary disorders and sepsis. Patients received high-dose intravenous corticosteroids, usually in conjunction with relatively low to moderate doses of neuromuscular junction-blocking agents. After discontinuation of the latter drugs, most had diffuse, flaccid weakness with failure to wean frommechanical ventilation. Electrodiagnostic findings were consistent with a necrotizing myopathy. Muscle histopathology revealed myopathy with loss of thick filaments in 79%, mild myopathic changes in 14%, and atrophy of type 1 and type 2 fibers in 7%. Loss of thick filaments was identified in muscle biopsy specimens obtained 30 ± 11 days (mean ± standard deviation) after intravenous corticosteroid treatment but not in those obtained earlier (12 ± 2 days). Critically ill patients, including those receiving organ transplants, may develop acute myopathy of intensive care after exposure to intravenous corticosteroids and neuromuscular junction-blocking agents, although the exposure to the latter drugs may be minimal. Selective loss of thick filaments is common in acute myopathy of intensive care, especially if the muscle biopsy specimen is obtained 2 weeks or more after intravenous corticosteroid exposure.

Acute myopathy of intensive care : Clinical, electromyographic, and pathological aspects

Critical care myopathy: an electrophysiological and histological study.

values P < 0Æ05. The JAK2 mutation was identified in 48% of our ET population, which is a similar frequency to those reported by others. There was no difference in age at diagnosis, gender or disease duration between those with and those without the mutation. The proportion of patients receiving some form of cytoreductive therapy was also similar in both the groups. However, we found a significantly higher haemoglobin concentration at diagnosis in ET patients with the mutation (median 14Æ2 ± 1Æ5 g/dl vs. 13 ± 1Æ7 g/dl, P 1⁄4 0Æ0426) although no differences were seen in the packed cell volume, white cell or platelet counts. Thrombotic complications were more common in patients with the JAK2 mutation; 18 (62%) vs. 8 (26%), P 1⁄4 0Æ009. Although arterial events were more common, overall there was no statistical difference between the two groups, as defined by JAK2 mutational status, for either the type or timing of the thrombotic event. Our data therefore suggests that the presence of the JAK2 mutation in ET defines a subgroup of patients with both a polycythaemic and thrombotic tendency, confirming the results of recent studies. The ease of screening for the V617F mutation makes it a very attractive tool for diagnostic purposes but its role in risk stratification for therapy remains to be further evaluated.

Central nervous system graft-versus-host disease post allogeneic stem cell transplant.

We read with interest the paper by Norton et al 1 showing an association between distal symmetric polyneuropathy and Mycobacterium avium complex (MAC) infection but not between distal symmetric polyneuropathy and cytomegalovirus (CMV) infection. This confirms our findings presented in Sydney in 1994,2 to be published later this year.3 

In our study a cohort of 94 consecutive …

Association between HIV distal symmetric polyneuropathy and Mycobacterium avium complex infection

An analysis of factors associated with HIV-related peripheral neuropathy

Chapter 2 – Catastrophic and sinister headache

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