Severe malaria complicated by circulatory shock is known as algid malaria. Cases of severe imported malaria are seen increasingly frequently in emergency departments in the United States, Europe, and other locales. The optimal volume resuscitation strategy for patients with severe malaria is not well-defined. A 20-year-old woman, who immigrated 2 weeks ago from Niger, Africa, presented to the emergency department of an urban teaching hospital with fever, hypotension, and malaise. She was resuscitated with 5.5 L of normal saline solution and norepinephrine. Thin blood smear demonstrated Plasmodium falciparum with parasitemia of 10% to 15%. She had rapid reversal of circulatory shock, cleared her parasitemia in less than 48 hours with antimalarial therapy, and was discharged home on hospital day 6 in good condition. The optimal resuscitation strategy for algid malaria is unknown, and volume restriction has been advocated as a means to prevent life-threatening cerebral and pulmonary edema. Although not identical, the late inflammatory response in severe malaria leading to capillary permeability shares many similarities with the immunologic response in bacterial sepsis. Our case report discusses a patient with severe imported malaria complicated by shock, successfully managed with large-volume fluid resuscitation, hemodynamic optimization, early antimalarial agents, and broad-spectrum antibiotics. This report questions the strategy of cautious fluid resuscitation in algid malaria and suggests that case series comparing goal-directed resuscitation to historic controls along with prospective multicenter controlled trials should be conducted to determine the best fluid resuscitation strategy.

Two patients with malaria due to Plasmodium falciparum who progressed to shock syndrome are reported. They received hemodynamic support in an intensive care unit without using antibiotics and presented improvements. Algid malaria should be a syndromic diagnosis of varying etiology (dehydration, bacterial infection, bleeding and/or adrenal insufficiency).

Algid is a rare complication of tropical malaria and it occurs in 0.37% of cases. Algid malaria is characterized by hemodynamic disorders as shock with pronounced metabolic changes and hypothermia. A number of factors are involved in the development of algid malaria. These include: 1. Pathological phenomena that are associated with the changes in the state of red blood cells and lead to impaired microcirculation (cytoadherence, sequestration, rosetting); 2. Tumor necrosis factor (TNF) that provokes hypoglycemia, coagulopathy, and impaired erythropoiesis; 3. Altered acid-alkali balance with the development of metabolic acidosis; 4. Gastrointestinal lesion. Adherence of contaminated red blood cells in the intestinal mucosal vessels induces epithelial ischemic damage. Impaired absorption of liquid and its loss with vomiting and diarrhea result in acute hypovolemia; 5. Algid malaria is associated with the addition of gram-negative septicemia. The paper describes a case of algid malaria.

This is a retrospective study on 7,005 cases of malaria treated in a base hospital during the period 1998 to 2001. The aim of the study is to analyze the patterns, complications and mortality rates of malaria and its response to standard anti-malarial drugs. Diagnosis of malaria was made from identification of parasites on Giemsa stained thick and thin blood slides among the febrile cases and the clinical (unspecified) malaria was diagnosed as per WHO criteria. Malaria cases accounted for 136.17 per thousand-hospital admissions. Out of 7,005 malaria cases, 54.22% were falciparum, 26.18% were vivax and 12.02% were mixed infections. The most common complications of falciparum malaria were cerebral malaria (2.80%), malarial hepatitis (1.55%), acute pneumonia and/or pulmonary edema (0.22%), acute renal failure (0.13%), algid malaria (0.13%) and black water fever (0.06%). Most of the cases (66.98%) responded (S-response) well to chloroquine. Among the rest, 11.99% required quinine, 9.79% required artemether and 0.08% required both mefloquine and artemether. The total mortality rate was 0.30% but it was 9.25% and 6.17% among complicated malaria and cerebral malaria cases, respectively. Prognosis appeared better on early recognition of complications and initiation of prompt, effective treatment and adequate nursing care. Most mortality was due to complicated falciparum malaria and the emergence of drug resistance.

Falciparum malaria presents with protean manifestations and is associated with a variety of complications and has a high mortality. One hundred and fifty-eight consecutive cases of falciparum malaria were studied with respect to the clinical presentation, complications, and response to treatment. The mean age of patients was 38.60 +/- 15.45 years and majority of them were males i.e., males being 110 (69.62%) and females being 48 (30.37%). The commonest presenting manifestations were fever with chill and rigor (98.10%), altered sensorium (48.10%), algid malaria (18.35%), and jaundice (27.21%). The other presenting features being oliguria (6.96%) and bleeding manifestations due to disseminated intravascular coagulation (DIC) (4.43%). The frequently encountered complications were anaemia (74.68%), jaundice (40.50%), cerebral malaria (45.56%), thrombocytopenia (40.50%) and renal failure (24.68%). Most of the patients i.e., 126 (79.74%) recovered with treatment and 32 (20.25%) succumbed. Higher mortality was associated with higher parasite count, presence of complications like anaemia, jaundice, renal failure, DIC, adult respiratory distress syndrome (ARDS), and septicaemia. Most of the deaths were encountered in patients where there was delay in clinical diagnosis, in the pre-hospital phase, and consequent presentation in multiorgan failure. Early diagnosis and institution of specific therapy were rewarding in the remaining patients in this series.

Severe and complicated malaria is an important cause of mortality in Plasmodium falciparum infection. We describe in this study the details of 532 cases of such syndromes admitted to hospital during an outbreak of malaria between September-December 1994. Increase in the annual rain fall, collection of water around Indra Gandhi Canal, forestation of shrubs around it and migration of labor, adaptation of Anopheles stephensi to desert climate and favorable breeding of An. culicifacies in the areas under impact of irrigation were presumptive causes of the outbreak in this region. Cerebral malaria (25.75%), hepatic involvement (11.47%), spontaneous bleeding (9.58%), hemoglobinuria (7.89%), severe anemia (5.83%), algid malaria (5.26%), ARDS (3%) and renal failure (2.07%) were the important manifestations. The overall mortality was 11.09%, which was high because of infection in the non-immune population of this area. Ignorance about the severity of this disease and lack of transportation facility was another important factor. Morality was highest in ARDS (81.25%) followed by severe anemia (70.97%), algid malaria (46.43%), renal failure (45.45%), jaundice (36.06%) and cerebral malaria (33.57%). Pregnancy was an important determinant increasing the mortality in female patients. Mortality was very high (82.35%) in those persons who presented with more than 3 syndromes together.

Resurgence of malaria has been noted in the Rohtak district (Haryana, India) after the recent floods. The profile of 66 patients of P. falciparum infection who were admitted to our hospital over one month in October 1995 is reported. While only a minority of cases (< 15%) presented with an uncomplicated course, all others developed one or more complication(s), some of them very rare. The usual manifestations viz, cerebral malaria, black water fever and algid malaria seen in the past were observed in less than half the patients. The remaining presented with unusual complications like haemolytic anaemia (46.2%), severe anaemia (37.9%), thrombocytopaenia (18.2%), pancytopaenia (6%), adult respiratory distress syndrome (4.5%) often not seen in sporadic cases of falciparum malaria which occurred in the past in this district. Similarly all deaths (15.1%) were noted in patients with rarer manifestations and only one patient died of cerebral malaria. This study confirms the occurrence of severe and complicated falciparum malaria in this part of the country.

Malaria, the most important of all tropical diseases, causes approximately one million deaths per year. In Plasmodium falciparum malaria, the organs most affected are the brain, kidneys, lungs, and liver. Cerebral involvement is the most important lethal complication with a mortality rate of up to 50%. We report a patient with malignant, tertian falciparum malaria with an initial parasitemia rate of 60% and severe cerebral, hepatorenal, and pulmonary involvement. In addition to the severe diffuse encephalopathy, an initial neurologic examination showed signs of a pontine lesion that was confirmed by cerebral magnetic resonance imaging. We therefore conclude that cerebral malaria may be responsible for focal neurologic lesions that can be demonstrated by this procedure.

Plasmodium falciparum malaria is endemic in the northern KwaZulu areas of South Africa. The clinical morbidity produced by this parasite has not been studied since the institution of the present malaria control programme. Fifty-nine patients were prospectively studied at a peripheral clinic during the peak malaria season; symptoms and signs of the infection, parasite loads, haemoglobin values and leucocyte counts were recorded in all patients. Haemoglobin and leucocyte counts were also measured in 37 control subjects without malaria. The commonest symptoms were persistent headache (100%), rigors (98%) and myalgia (93%). None of the patients presented with coma, pulmonary oedema, hypoglycaemia or algid malaria. Splenomegaly was found in 49%, hepatomegaly in 20% and mental confusion in 5% of patients. Mean parasite load was 1.71% and 57% of patients had parasite loads of < 1%. Anaemia of < 10 g/dl was significantly more frequent (P < 0.0001) in the patient group than in the control group. Leucopenia (white cell count < 4.0 x 10(9)/l) was present in 12 of 50 patients in whom it was measured compared with 2 controls (P = 0.0175). The results show a wide range of morbidity, without severe complications as presenting manifestations. Symptomatic infection in the presence of low parasite loads suggests that there may be little or no immunity in this population.

Two cases of cerebral malaria with hyperkinetic shock are reported. The first case concerned a 39-year-old european male who was not taking any prophylactic anti-malarial drugs. After having had headache and fever for a week, he was admitted to the intensive care unit (ICU) in coma and with jaundice. His initial systolic blood pressure was 60 mmg, with a central venous pressure (CVP) of -3 cmH2O. Five-hundred ml of modified fluid gelatin increased the CVP without raising the blood pressure. Haemodynamic investigations revealed a cardiac index (CI) = 5.2 l.min-1.m-2, peripheral arterial resistances (Rsa) = 290 dyn.s.cm-5, oxygen consumption (VO2) = 120 ml.min-1.m-2. Despite treatment with dopamine and dobutamine, the patient died 3 h after his admission, with a CI of 1.9 l.min-1.m-2. The second patient was a 14-year-old senegalese girl, admitted in circumstances similar to the first case. Initial haemodynamic investigations gave the following figures: CI 6.5 l.min-1.m-2, Rsa = 476 dyn.s.cm-5, VO2 = 174 ml.min-1.m-2. Recovery was obtained with fluid replacement therapy and dopamine. In the absence of another associated infectious disease, the plasmodial origin of the septic shock would seem to be the most likely in both cases. Pathophysiological mechanisms of these algid forms of malaria remain enigmatic. Various factors are discussed: cytoadherence of erythrocytes infected with Plasmodium falciparum, immunological disturbances, or a specific endotoxin.

In the treatment of severe Plasmodium falciparum infection antimalarial drugs should, ideally, be given by controlled rate intravenous infusion until the patient is able to swallow tablets. In cases where infection has been acquired in a chloroquine resistant area, and where it has broken through chloroquine prophylaxis or where the geographical origin or species are uncertain, quinine is the treatment of choice. When access to parenteral quinine is likely to be delayed, parenteral quinidine is an effective alternative. A loading dose of quinine is recommended in order to achieve therapeutic plasma concentrations as quickly as possible. In the case of chloroquine sensitive P. falciparum infection, chloroquine, which can be given safely by slow intravenous infusion, may be more rapidly effective and has fewer toxic effects than quinine. There is limited experience with parenteral administration of pyrimethamine sulphonamide combinations such as Fansidar, and resistance to these drugs has developed in South East Asia and elsewhere. Mefloquine and halofantrine cannot be given parenterally. Qinghaosu derivatives are not readily available and have not been adequately tested outside China. Supportive treatment includes the prevention or early detection and treatment of complications, strict attention to fluid balance, provision of adequate nursing for unconscious patients and avoidance of harmful ancillary treatments. Anaemia is inevitable and out of proportion to detectable parasitaemia. Hypotension and shock ('algid malaria') are often attributable to secondary gram-negative septicaemia requiring appropriate antimicrobial therapy and haemodynamic resuscitation. Many patients with severe falciparum malaria are hypovolaemic on admission to hospital and require cautious fluid replacement. Failure to rehydrate these patients may lead to circulatory collapse, lactic acidosis, renal failure and severe hyponatraemia.(ABSTRACT TRUNCATED AT 250 WORDS)

In Africa, the obstetrical risk is related to the difficulty to monitor the pregnancy during which obstetrical emergency may occur and will have to be treated by the practitioner with, sometimes, inadequate facilities. The authors examine the problems concerning successively the expectant mother, the foetus and the placenta. Then, they propose some solutions in the field of anesthesia and intensive care. The expectant mothers are exposed to the heat and sometimes are suffering from undernutrition, so it requires special attention when using anesthetics. In addition, they frequently present an increased morbidity:--universal diseases among which renovascular syndromes often lead to eclampsia and to abruptio placentae;--tropical diseases may raise problems either to anesthesia (sickle cell anemia, bilharziosis) or to intensive care (algid pernicious fever, malignant amebiasis). Children are subject to an increased stillbirth rate in accordance with pregnancy duration and with the intensive facilities available at the time of the birth. Either infective or mechanical complications may occur in placenta and they may cause some distress to both mother and foetus. With respect to all these cases, the authors examine the various analgesia methods for obstetrical purpose and point out their indications and contraindications. It seems that regional anesthesia is suitable for health posts without facilities. Peridural anesthesia is operative with a great number of situations but it requires some technical training. Then methods to monitor both mother and foetus are exposed. According to the available facilities, ways and means are given to solve problems of anesthesia: labour maternal complications (Mendelson's syndrome, eclampsia, obstetrical complications either mechanical and hemorrhagic) or secondary complications (bacterial or parasitic complications, renal insufficiency); foetal complications either during labour, or at birth, or after delivery.

Fluorescent cytochemical techniques, chiefly end-group methods, have been employed in the characterization of cells in calid and algid normal and LUCKE tumor-bearing kidneys of the leopard frog, Rana pipiens. Cytoplasmic RNA and glycogen distribution reflect the known patterns of general metabolic activity of the respective cells in question. Protein sulfhydryl distribution is similar in normal distal tubules and tumors while both differ significantly from proximal tubules. Viral inclusions in nuclei of algid tumor cells contain demonstrable DNA, protein sulfhydryls and disulfides, arginine and lysine-rich basic proteins, also both C-terminal and side chain carboxyl groups. Significant amounts of DNA are demonstrable in the cytoplasm of algid tumors. Fluorescence cytochemical methods directed toward end-groups or specific classes of macromolecules offer a particularly favorable option, because of increased sensitivity and higher levels of contrast, for comparative cytological investigations of the LUCKE tumor and of similar systems.