Ronald C. Allison

The Other Medical Causes of Rhabdomyolysis

&NA; Rhabdomyolysis is the clinical and laboratory syndrome resulting from skeletal muscle injury and release of potentially toxic substances into the circulation. The severity of rhabdomyolysis varies widely from asymptomatic elevation of muscle enzymes to the life‐threatening complications of acute renal failure and severe electrolyte abnormalities. The etiology of rhabdomyolysis may be considered under 4 categories: (1) trauma or direct injury, (2) excessive muscle activity, (3) hereditary muscle enzyme defects, and (4) other less obvious medical causes. The latter medical causes may be subdivided into the following: (1) drugs and toxins, (2) muscle hypoxia, (3) metabolic and endocrine disorders, (4) infections, (5) temperature alterations, and (6) miscellaneous causes. The diagnosis of rhabdomyolysis depends on recognizing the symptoms of muscle pain and weakness, detecting the presence of or history of red‐to‐brown urine (myoglobinuria), and finding short‐term elevations of creatine kinase that are not attributable to myocardial infarction or inflammatory myopathies. The major therapeutic goal is to recognize and treat complications as soon as possible, particularly electrolyte abnormalities and acute renal failure. Knowledge of the other medical causes of rhabdomyolysis allows one to identify and treat this potentially serious condition in otherwise occult cases.

Measurement of effective pulmonary capillary pressure using the pressure profile after pulmonary artery occlusion.

Pulmonary artery catheters are frequently used to measure pulmonary vascular pressures, particularly the pulmonary wedge pressure (Pw), which reflects pulmonary venous and ideally left atrial pressures. However, the pulmonary capillary pressure (Pc) is the major force in the formation of pulmonary edema. Unfortunately, Pw has been interpreted as being identical to Pc. In this study we used 7-Fr pulmonary artery catheters to measure effective Pc in closed-chest animals and patients. The decreasing pressure profile after pulmonary artery occlusion was separated into fast and slow components, with the inflection point between them representing Pc. Pc was also estimated by mathematically analyzing the curves in terms of a precapillary resistance, a large pulmonary capillary capacitor, and a postcapillary resistance.In dogs, Pc was determined after pulmonary vascular resistance had been increased by infusing serotonin and histamine. While Pw remained unchanged, serotonin increased pulmonary artery pressure (Ppa) 52% and Pc 16%, whereas histamine increased Ppa only 25%, but increased Pc by 35%. This is consistent with studies showing that serotonin primarily elevates precapillary resistance, and histamine increases postcapillary resistance.In thoracic surgery patients, Pc was not consistently related to Pw. This measurement was simple, reproducible, and provided a more precise capillary filtration pressure than Pw. It should be clinically useful in monitoring patients with pulmonary hypertension and adult respiratory distress syndrome, especially those with pulmonary artery catheters.

Pulmonary edema: Complication in the management of sickle cell pain crisis

Over a 12-month period, there were 51 admissions for sickle cell pain crisis. Of these, the course of four patients (two with hemoglobin SS, one with hemoglobin SC, and one with hemoglobin S-Thal) was complicated by the development of pulmonary edema. Pulmonary edema complicating the management of sickle cell pain crisis has not previously been described. Vigorous fluid replacement with hypotonic saline and parenteral narcotic analgesics are conventional modalities of therapy, but may contribute to the development of pulmonary edema. Narcotic analgesics causing increased permeability are well established. In pulmonary vascular beds predisposed to injury, hypotonic saline administration causing an increased hydrostatic pressure and decreased oncotic pressure may further compound pulmonary edema development. On the basis of the experience in this study, a conservative approach to the use of fluid administration and narcotic analgesics is advised.

Initial treatment of pulmonary edema: a physiological approach.

An understanding of the physiological principles involved in lung fluid balance is useful in the initial treatment of pulmonary edema. Normally, a very small volume of fluid is filtered from the pulmonary vasculature into the interstitial space. This interstitial fluid enters the pulmonary lymphatics and is transferred to mediastinal lymphatics at an estimated rate of 20 ml/hr. Under abnormal circumstances, fluid filtration may occur at such a rapid rate that it overwhelms the lymphatics and interstitial space and results in alveolar flooding. This may occur as a result of increased pulmonary vascular pressure or increased vascular permeability. The two general goals of initial therapy are (1) to relieve hypoxemia and (2) to reduce pulmonary capillary pressure. Relieving hypoxemia may require the use of supplemental oxygen by nasal prongs or mask, continuous positive airway pressure (CPAP) mask, or even endotracheal intubation and mechanical ventilation. Measures to decrease preload and thereby reduce pulmonary capillary pressure include sitting the patient up, administering a loop diuretic or morphine intravenously, and in some circumstances using sublingual nitroglycerin. After initial treatment is underway, a search for and specific management of the underlying cause of pulmonary edema can proceed.

Changes in the pulmonary capillary pressure after cardiac surgery

The changes in the pulmonary circulation in 37 cardiac surgery patients undergoing coronary artery bypass (CABG), n=16; aortic valve replacement (AVR), n=13; and mitral valve replacement (MVR), n=8 were studied. The visual technique for the determination of pulmonary capillary pressure (Pc) was used in the preoperative and postoperative periods. The ratio of Pc to the pulmonary artery wedge pressure (Pw) was calculated to determine whether Pc and Pw varied independently. In addition, total pulmonary vascular resistance (PVR) was divided into precapillary (ra) and postcapillary (rv) components. Results from the CABG patients showed that the relationship between Pc and Pw remained constant despite an increased cardiac output. This differs from the data obtained from AVR and MVR patients in whom the Pc/Pw ratio was significantly higher after surgery. Therefore, Pw would underestimate Pc in this group of patients. In addition, MVR patients showed a significant postoperative increase in PVR and rv as compared with their preoperative values. This was also significantly higher than the rv in either AVR or CABG patients. The etiology of this change is unknown.

Pulmonary Capillary Blood Pressure

When one considers the various vascular pressures throughout the body’s circulation, it is remarkable that the lungs’ circulation is such a high-flow circuit with low resistance. In addition, in various types of lung pathology it is even more remarkable that the alveoli do not easily fill with fluid, which would compromise the gas exchange function of the lung. For many years, it was thought that the pulmonary microvascular pressure was quite low because the average pulmonary systolic pressure is about 20–25 mm Hg and pulmonary diastolic pressure is approximately 10–15 mm Hg. Since left atrial pressure is only 0–5 mm Hg, capillary pressure was estimated to be approximately 5–10 mm Hg. However, it was not until 1967 that Gaar et al. applied the isogravimetric technique developed by Pappenheimer and Soto Rivera (1948) to the isolated dog lung to measure pulmonary capillary pressure.