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An epidemic of dengue type 2 which occurred on Niue Island during the first half of 1972 involved approximately 90% of the population of 4,600 persons and affected all age groups equally. Serologic data indicated that this was the first occurrence of any dengue virus on the island for at least 25 years. Many persons had minor hemorrhages associated with febrile illnesses during the outbreak and a few had severe hemorrhages or shock. Twelve deaths occurred which may have been caused by dengue. The clinical features of the fatal illnesses among children were very similar to those described previously for dengue hemorrhagic fever or dengue shock syndrome. It is concluded that at least some deaths among children were caused by dengue virus and were, consequently, the result of primary infection with that virus.

THE third endogenous catecholamine, dopamine, has been extensively investigated in recent years. Dopamine, the immediate precursor of norepinephrine, is found in high concentrations in sympathetic ...

The simultaneous regression of vascular resistance ( R ) on oxygen transport ( T ) and haematocrit ( H ) was studied in the total systemic and femoral circulations in normal sheep and in normal and shocked greyhounds. The regressions of R and T on H were different in normal greyhounds and sheep. In the greyhound the regressions were profoundly modified by the state of the circulation and within the range of these observations no evidence was obtained to support the concept of ‘optimum' haematocrit.

✓ Cerebral oxygen metabolism was studied in the dog at brain temperatures ranging from 37° to 8°C. As brain temperature decreased, the cerebral oxygen metabolism (CMRO2) decreased following the Arrhenius equation. The natural logarithm of the CMRO2 was a linear function of the reciprocal of the absolute (K) brain temperature. Oxygen metabolism, although much decreased, continued at very low brain temperatures. The CSF composition was unchanged after 1 hour at brain temperatures down to 10°C. Circulatory arrest for tolerable periods and longer caused changes only in the CSF potassium concentration. The interval between the onset of circulatory arrest and the beginning of the CSF K concentration increased with decreasing temperature and the rate of CSF K increase was increasingly slower at lower temperatures. At all temperatures the rate of CSF K changed gradually increased with time. The interval before the CSF K started to increase was dependent upon the amount of O2 available in the brain and the length of this interval was inversely proportional to the CMRO2. The amount of CSF K concentration was not clearly related to the tolerable periods of circulatory arrest, but at normal temperatures an obviously increased CSF K following a period of acute cerebral anoxia without CSF hemorrhage may indicate brain damage.

Experience with 144 cases of blunt and penetrating renal injuries encountered from1967 to 1973 has been analyzed and compared with data collected from the literature. The following points are emphasized: (1) importance of preoperative radiographic assessment, (2) limited number of indications for surgical intervention, and (3) encouragement of conservatism in marginal or inconclusive cases. Discounting cases surgically explored unnecessarily and cases with serious or lethal nonurologic trauma precluding repair of major renal injuries, our data predict a need for surgical intervention in 37 per cent of all cases of renal trauma; surgical intervention was required in 37 per cent with blunt injuries and 45 per cent with penetrating lesions.

This paper is a contribution to the study of the surgical treatment of subtrochanteric fractures. By the term ‘subtrochanteric fractures’ we mean fractures beginning at or directly below the lesser trochanter and extending down the shaft of the femur.

The arterial to end-tidal Pco2 gradient was measured in normal subjects and in the following patient groups: acute pulmonary embolism, acute myocardial infarction, left ventricular failure, pneumonia, obstructive lung diseases, primary pulmonary hypertension and shock from various causes. Increased gradients were observed in 24 of 25 patients with moderate or massive embolism, in 7 of 17 with small emboli, in 20 of 34 with chronic lung diseases, in 6 of 14 with shock and in 3 of 24 with left ventricular failure. By measuring in maximal expiration, high gradients in lung embolism were only slightly reduced, but approached zero in obstructive lung diseases or left ventricular failure. The patients with large emboli were thus clearly separated from other groups with acute or chronic ventilation-perfusion disturbances. No conclusive results were obtained in patients in shock.

A singularly effective guide to the evaluation and early care of burn injury, emphasizing the importance of fluid resuscitation, is presented here. Although controversy still exists regarding the types of fluid that should be used, the authors and others treating major burns agree that sodium is essential.Other commonly used systems for fluid resuscitation are the Evans, Brooke, and MGH formulas. Their rationale and use are discussed in “The Treatment of Burns” by C. P. Artz and J. A. Moncrief (W. B. Saunders Co., Philadelpha, 1969) and “Contemporary Burn Management” by H. C. Polk, Jr., and H. H. Stone (Little, Brown and Co., Boston, 1971).Two important points to remember in burn management are (1) learn one system and use it well and (2) remember that any formula is useful only as a guide and must be modified if necessary.—MSR

The problem of sudden and unexpected death after the parenteral administration of a therapeutic dose of choloroquine in fibrile patients was investigated using rabbits. Hyperthermia was produced in both conscious and anaesthetized rabbits using a Megatherm Junior diathermy machine. Lead II of the electrocardiogram, respiration and blood pressure were monitored during slow i.v. injection of chloroquine. In hyperthermic rabbits, striking cardiac arrhythmias, circulatory collapse and death occured at a dose level 13 as great as in normal rabbits. Animals that had been heated and allowed to cool before the injection, tolerated 23 of the lethal dose for normal rabbits, and twice as much as the hyperthermic rabbits.

The inadequate circulatory profusion states collectively called shock are summarized. Shock a condition in which circulation is inadequate for normal cellular function may be classified as: 1) hypovolemic 2) septic 3) cardiogenic 4) anaphylactic 5) due to impeded blood flow 6) endocrine and 7) neurogenic. The physiologic changes common to all forms of shock are outlined and each of the 7 types of shock are discussed separately. Treatment of shock includes measurement of central venous pressure to assess the function of the right side of the heart and the need for fluid replacement. After intravenous lines are secured (techniques described) electrolyte solution is administered at a rapid rate until the central venous pressure rises 5 cm of water above the base line measurement. Use of a Foley catheter to measure urinary output an indirect measure of renal perfusion is recommended. Arterial monitoring is also widely used in care of patients in shock. Since shock is also concerned with relative cellular hypoxia oxygen should be given as soon as possible. Treatments related to particular types of shock are outlined individually with the goal of all to restore and maintain adequate cellular perfusion. Vasopressors worsen the already impaired peripheral circulation in shock and have no place in the treatment except occasionally in cardiogenic shock when their positive inotropic effect may be helpful.

The advent of neonatal intensive care units has led to familiarity with problems of alveolar instability, ventilation-perfusion inequality, airway obstruction, and interstitial disease, all of which may be seen in infants who must have surgery in the newborn period. The basis of these advances has been an increased understanding of infant pulmonary physiology.

Shock may be initiated by cardiac failure, hypovolaemia, or a primary change in peripheral resistance or venous capacitance vessels. Most of the clinical signs of shock occur as a result of sympatho-adrenal stimulation and peripheral tissue anoxia. Typically animals show an altered level of consciousness, tachycardia, poor peripheral perfusion (shown by a prolonged capillary refilling time) and poor organ perfusion (shown by oliguria). Cardiogenic shock is characterized by a fixed low cardiac output, hypotension, increased systemic resistance and an elevated central venous pressure. With hypovolaemic shock, central venous pressure, cardiac output and blood pressure fall while systemic resistance increases. Vasculogenic shock presents a varied clinical picture and there may be evidence of vasodilatation or vasoconstriction in mucous membranes. The haematocrit rises and there is rapid development of a marked metabolic acidosis. Resume. Un choc peut s'indiquer par un arret du caeur, une hypovolemie, ou un changement primaire dans la resistance capillaire ou la capacite veineuse. La plupart des manifestations cliniques de choc se produisant comme resultat d'une stimulation sympatho-surrenale et d'une anoxie des tissus peripheriques. D'une maniere typique, on note chez les animaux un niveau altere de toute leur connaissance, une tachycardie, une faible perfusion peripherique (indiquee par un temps prolonge de remplissage capillaire) et une faible perfusion des organes (indiquee par une uropenie). Un choc cardiogene se caracterise par un fonctionnement cardiaque fixe et au ralenti, une hypotension, une resistance accrue du systeme et une pression veineuse elevee et centrale. Avec un choc hypovolemique, la pression veineuse centrale, le fonctionnement cardiaque et la tension baissent tandis que la resistance du systeme s'accroit. Le choc vasculogene presente un ensemble varie de protocoles d'observation et il peut y avoir evidence de vasodilatation ou de vasoconstriction dans les membranes muqueuses. L'hematocrite s'eleve et une acidose metabolique marquee se developpe rapidement. Zusammenfassung. Schock kann sich in Herzschlag, Hypovolamie oder in einer primaren Anderung im Kapillanviderstand oder in venoser Kapazitat zeigen. Die meisten klinischen Anzeichen von Schock erscheinen als das Ergebnis von sympatho-adrenaler Stimulation und peripher Gewebeanoxie. Es ist typisch, dass die Tiere ein verandertes Mass von Bewusstsein, Tachykardie, schlechte periphere Perfusion, die sich in einer verlangerten kapillaren Fullungszeit und schlechter Organperfusion, wie Oligurie, zeigen. Kardiogenischer Schock ist charakterisiert in starrem niedrigem Herzausstoss, Hypotonie, zunehmender systemischer Resistanz und einem erhohtem zentralem venosem Druck. Mit hypovolamischen Schock fallen zentraler venoser Druck, Herzausstoss und Blutdruck, wahrend systemische Resistanz zunimmt. Vaskulogenischer Schock stellt ein verschiedenes klinisches Bild dar und Gefasserweiterung oder Gefassverengerungen konnten sich beweisen. Der Hamatokrit steigt und es gibt eine rapide Entwickling von einer gekenntzeichneten metabolischen Acidose.

This study tests the hypothesis that ventricular geometry at low preloads (near empty ventricles) impairs diastolic regional coronary flow and, therefore, plays a role in production of myocardial ischemic injury observed after cardiopulmonary bypass and hypovolemic shock. There was no effect of preload on the left ventricular transmural distribution of diastolic coronary resistance. It is concluded that this is not the mechanism of myocardial injury in normal hearts.

Echis carinatus is the most important cause of morbidity and mortality from snake bite in Nigeria and in many other parts of the world. Forty-six patients with systemic poisoning by this snake were given echis antivenom made either by the South African Institute for Medical Research (S.A.I.M.R.) or by Behringwerke (North and West African polyvalent antivenom). A simple test of blood coagulability was used to assess whether an adequate neutralizing dose of antivenom had been given. An average of 15.2 ml S.A.I.M.R. antivenom restored normal coagulability permanently in all 23 patients in one group, but in the other group receiving an average dose of 37.9 ml Behringwerke antivenom normal clotting resulted in only 18 out of 23 patients. Local tissue swelling was similar in both groups, but local necrosis occurred in three patients treated with Behringwerke antivenom and in none given S.A.I.M.R. antivenom.

MDF is a small peptide, having a molecular weight of 500–1000 that is produced in the ischemic pancreas during a variety of types of circulatory shock. It is probably produced by the proteolytic degradation of intracellular pancreatic protein by the combined action of lysosomal and zymogenic proteases. MDF is transported to the circulation by lymphatics and by systemic microcirculatory vessels. MDF depresses contractility of the heart under a variety of hemodynamic conditions. It also constricts splanchnic resistance vessels thereby favoring its production. Moreover, this toxic peptide contributes to reticuloendothelial phagocytic depression thus hampering its clearance from the circulation. Glucocorticoids and certain protease inhibitors are very effective pharmacological agents in preventing the formation of MDF. Conventional inotropic agents are not ideal agents in shock since they usually exert undesirable side effects which cancel much of their useful inotropic action. Surgical interventions such as pancreatic duct ligation, pancreatectomy, pancreatic vascular perfusion, thoracic lymph duct diversion or hemodialysis can prevent the formation, transport, or biological actions of MDF in animals, but they are impractical and difficult to perform in patients during shock. MDF is a toxic factor that contributes to the lethality of the shock state by virtue of its positive feedback actions. Moreover, lysosomal hydrolases which are released into the circulation during shock are directly deleterious to the organism, and also sensitize the circulatory system to the deleterious effects of MDF. Further work is needed to determine the complete chemical identity of MDF and to evaluate its detailed mechanism of action in shock states. Therapeutic measures specific for the antagonism of MDF would be a desirable and useful tool in the overall therapeutics of many types of circulatory shock.

Although the life-threatening emergencies discussed here—interference with oxygenation, circulatory failure, and severe hemorrhage—are most often found in the traumatized patient, they occur in the acutely ill as well. The progressive methods outlined for dealing with them are applicable to any patient with a serious injury or illness, are very flexible, and allow the physician to concentrate on the major injuries yet not ignore other possible injuries.—MSR