PubMed Health⌕ Search
Home/Archive/PubMed

PubMed · 378543

Multisystem failure: a review with special reference to drowning.

B H Hoff
View original source ↗Export metadata ↓

Abstract

Near-drowning represents an insult that can affect all organ systems. A common pathway for injury is hypoxemia, acidosis, and hypoperfusion. Pulmonary insufficiency and CNS dysfunction are major causes of morbidity and mortality. Variations in vascular volume, heart failure, renal failure, coagulation disorders, and electrolyte disturbances may also be present. Patients should be observed for multisystem failure and therapy tailored to the particular needs of each victim.

Explore related subjects

AcidosisAcute Kidney InjuryAdultBlood Coagulation DisordersBlood PressureBody Temperature RegulationBrain EdemaCapillary PermeabilityCardiac OutputCentral Nervous System DiseasesCentral Venous PressureChildCritical CareDrowningHeart ArrestHumansHypothermiaHypoxiaImmersionIntubation, IntratrachealLungMyocardial ContractionOxygen ConsumptionPositive-Pressure RespirationPulmonary EdemaRespiratory Distress SyndromeRespiratory InsufficiencyWater-Electrolyte ImbalanceJournal ArticleReview

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

B H Hoff. 1979. Multisystem failure: a review with special reference to drowning.. https://pubmed.ncbi.nlm.nih.gov/378543/

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

PubMed2007

Grave acidosis after severe anaphylactic bronchospasm: friend or foe?

In a 20-year-old woman with known asthma, anaphylactic bronchospasm induced a grave combined respiratory and metabolic acidosis (pH(a) 6.66) with marked hypoxaemia (S(a)O(2) 45%). The beneficial effects of the rightward shift of the oxyhaemoglobin dissociation curve on tissue O(2) unloading at such pH was more than offset by the negative effect on S(a)O(2) at the reduced P(a)O(2) (7.0 kPa) found in this patient. This case illustrates the detrimental effect of grave acidosis on arterial blood oxygen content at subnormal P(a)O(2) values, the beneficial effect of a supranormal P(a)O(2) on the S(a)O(2) in such patients, and the rapid remission rate of life-threatening acidosis and blood lactate after adequate ventilation and tissue oxygenation were secured. The initial treatment of the patient and clinically relevant considerations are discussed.

Acidosis↗
PubMed2007

[Isoniazid intoxication].

HISTORY AND ADMISSION FINDINGS: A 55-year-old woman presented with sustained convulsions after the ingestion of an at first unknown amount of isoniazid, rifampin, ethambutol and alcohol. INVESTIGATION: At admission the patient had a severe metabolic acidosis. Blood tests showed changes caused by the hepatotoxicity of isoniazid. TREATMENT AND COURSE: Because diazepam was not efficacious in controlling the convulsions the patient was intubated. In response to the therapautic measures the convulsions stopped and metabolic acidosis was quickly compensated. Pyridoxine was given intravenously as an antidote. CONCLUSION: The rare intoxication with isoniazid demands immediate administration of pyridoxine and aggressive treatment of the convulsions.

Acidosis↗
PubMed2007

Mitogen-activated protein kinase-dependent activation of the Na+/H+ exchanger is mediated through phosphorylation of amino acids Ser770 and Ser771.

We investigated regulation of the type 1 isoform of the Na(+)/H(+) exchanger by phosphorylation. Four specific groups of serine and threonine residues in the regulatory carboxyl-terminal tail were mutated to alanine residues: group 1, S693A; group 2, T718A and S723A/S726A/S729A; group 3, S766A/S770A/S771A; and group 4, T779A and S785A. The proteins were expressed in Na(+)/H(+) exchanger-deficient cells, and the activity was characterized. All of the mutants had proper expression, localization, and normal basal activity relative to wild type NHE1. Sustained intracellular acidosis was used to activate NHE1 via an ERK-dependent pathway that could be blocked with the MEK inhibitor U0126. Immunoprecipitation of (32)P-labeled Na(+)/H(+) exchanger from intact cells showed that sustained intracellular acidosis increased Na(+)/H(+) exchanger phosphorylation in vivo. This was blocked by U0126. The Na(+)/H(+) exchanger activity of mutants 1 and 2 was stimulated similar to wild type Na(+)/H(+) exchanger. Mutant 4 showed a partially reduced level of activation. However, mutant 3 was not stimulated by sustained intracellular acidosis, and loss of stimulation of activity correlated to a loss of sustained acidosis-mediated phosphorylation in vivo. Mutation of the individual amino acids within mutant 3, Ser(766), Ser(770), and Ser(771), showed that Ser(770) and Ser(771) are responsible for mediating increases in NHE1 activity through sustained acidosis. Both intact Ser(770) and Ser(771) were required for sustained acidosis-mediated activation of NHE1. Our results suggest that amino acids Ser(770) and Ser(771) mediate ERK-dependent activation of the Na(+)/H(+) exchanger in vivo.

Acidosis↗