Relation of Colloid Osmotic Pressure to Arterial Hypoxemia and Cerebral Edema During Crystalloid Volume Loading of Patients with Diabetic Ketoacidosis

Fein, I. Alan; Rackow, Eric C.; Sprung, Charles L.; Grodman, Richard

doi:10.7326/0003-4819-96-5-570

Cited by 103 publications

(29 citation statements)

References 27 publications

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“…That many of our patients presented with altered level of consciousness before therapy was initiated vindicate the probable role of abnormal energy metabolism and metabolic derangements in diabetic ketoacidosis that results in abnormal biochemistry which also affects central neurological function (2). The idea that the treatment of DKA itself might be the cause of cerebral oedema has gained support over the years, but no single aspect of therapy has been implicated in studies to date, furthermore cerebral eodema has been shown to be present even before treatment begins (17,18).…”

Section: Discussionmentioning

confidence: 99%

Prognostic factors in patients hospitalised with diabetic ketoacidosis at Kenyatta National Hospital, Nairobi

Otieno

Kayima²,

Mbugua³

et al. 2010

E Af Med Jrnl

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Background: In spite of many advances in the management of diabetes in the last 25 years, the mortality associated with diabetic ketoacidosis (DKA) remains high, especially in the developing countries. The mortality appears greatest in the first 24 -48 hours of their treatment. Most of the previous studies on DKA focused on children and the precipitating factors thereof but not particularly on clinical predictors of outcomes. Objective: To determine the clinico-laboratory predictors of outcomes of patients hospitalised with diabetic ketoacidosis who were undergoing treatment. Design: Cross-sectional descriptive study. Setting: The accident and emergency department and medical wards of the Kenyatta National Hospital. Subjects: Fifty one patients hospitalised with diabetic ketoacidosis over a nine month period were evaluated clinically and by laboratory tests. They were managed in the standard way with insulin, intravenous fluids and appropriate supportive care. Main outcome measures: Serial assays of serum electrolytes, glucose and blood pH, HbA1c and clinical outcome of either discharge home or death. Results: Of the 51 patients enrolled, 47 were included in the final analysis. Fourteen (29.8%) patients died, and the deaths occurred within less than 48 hours of hospitalisation and treatment. Of the patients who died, all (100%) had altered level of consciousness at hospitalisation, 71.4% had abnormal renal functions, 64.3% were newly diagnosed and an equal proportion of 64.3% were females. The alteration in the level of consciousness was significantly associated systolic hypotension and severe metabolic acidosis, (p<0.001). Patients with altered level of consciousness also had poorer renal function. Conclusion: Apparently DKA still carries high mortality during treatment in hospital. Altered level of consciousness, which is an obvious and easily discernible clinical sign, was a major predictor of mortality in our study patients. The majority of patients with altered level of consciousness also had systolic hypotension, severe metabolic acidosis and impaired renal function. Even where and when detailed laboratory evaluation is elusive, clinical signs, especially altered level of consciousness and systolic hypotension are very important markers of severity of DKA that may be associated with unfavourable outcomes. Further studies are necessary to establish why DKA still carries high mortality in the patients who are already receiving treatment in hospitals in developing countries.

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Section: Discussionmentioning

confidence: 99%

Prognostic factors in patients hospitalised with diabetic ketoacidosis at Kenyatta National Hospital, Nairobi

Otieno

Kayima²,

Mbugua³

et al. 2010

E Af Med Jrnl

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“…During rehydration with fluid and electrolytes, an initially elevated colloid osmotic pressure is reduced to subnormal levels. This change is accompanied by a progressive decrease in arteriolar partial pressure of oxygen (PaO 2 ) and an increase in alveolar-to-arteriolar oxygen (AaO 2 ) gradient, which is usually normal at presentation in DKA (19,175,198). In a small subset of patients, this may progress to ARDS.…”

Section: Cerebral Edemamentioning

confidence: 99%

“…Significant decreases in the size of the lateral ventricles, as determined by echoencephalogram, were noted in 9 out of 11 DKA patients during therapy (198,199). However, in another study, nine children in DKA were compared with regard to brain swelling before and after therapy, and it was concluded that brain swelling is usually present in DKA before treatment is begun (200).…”

Section: Cerebral Edemamentioning

confidence: 99%

Management of Hyperglycemic Crises in Patients With Diabetes

et al. 2001

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Abbreviations: AaO 2 , alveolar-to-arteriolar oxygen; AKA, alcoholic ketoacidosis; ARDS, adult respiratory distress syndrome; BUN, blood urea nitrogen; CPT, carnitine palmitoyl-transferase; CSF, cerebrospinal fluid; DKA, diabetic ketoacidosis; FFA, free fatty acid; HHS, hyperosmolar hyperglycemic state; IRI, immunoreactive insulin; PaO 2 , arteriolar partial pressure of oxygen; RDKA, recurrent DKA.A table elsewhere in this issue shows conventional and Système International (SI) units and conversion factors for many substances. Management of Hyperglycemic Crises in Patients With Diabetes T E C H N I C A L R E V I E R e v i e w s / C o m m e n t a r i e s / P o s i t i o n S t a t e m e n t s 132DIABETES CARE, VOLUME 24, NUMBER 1, JANUARY 2001Technical Review noted in newly diagnosed obese type 2 diabetic patients (5,26,31). Therefore, the concept that the presence of DKA in type 2 diabetes is a rare occurrence is incorrect.The most common types of infections are pneumonia and urinary tract infection, accounting for 30-50% of cases (Table 4). Other acute medical illnesses as precipitating causes include alcohol abuse, trauma, pulmonary embolism, and myocardial infarction, which can occur both in type 1 and 2 diabetes (6). Various drugs that alter carbohydrate metabolism, such as corticosteroids, pentamidine, sympathomimetic agents, and ␣-and ␤-adrenergic blockers, and excessive use of diuretics in the elderly may also precipitate the development of DKA and HHS.The recent increased use of continuous subcutaneous insulin infusion pumps that use small amounts of short-acting insulin has been associated with an incidence of DKA that is significantly increased over the incidence seen with conventional methods of multiple daily insulin injections, in spite of the fact that most of the mechanical problems with insulin pumps have been resolved (6,(32)(33)(34). In the Diabetes Control and Complications Trial, the incidence of DKA in patients on insulin pumps was about twofold higher than that in the multipleinjection group over a comparable time period (35). This may be due to the exclusive use of short-acting insulin in the pump, which if interrupted leaves no reservoir of insulin for blood glucose control.Psychological factors and poor compliance, leading to omission of insulin therapy, are important precipitating factors for recurrent ketoacidosis. In young female patients with type 1 diabetes, psychological problems complicated by eating disorders may be contributing factors in up to 20% of cases of recurrent ketoacidosis (36,37). Factors that may lead to insulin omission in younger patients include fear of weight gain with good metabolic control, fear of hypoglycemia, rebellion against authority, and stress related to chronic disease (36). Noncompliance with insulin therapy has been found to be the leading precipitating cause for DKA in urban African-Americans and medically indigent patients (5,26). In addition, a recent study showed that diabetic patients without health insurance or with Medicaid alone had hospitali...

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“…CE occurs rarely in patients older than age 20 years (8,11,12), despite the presence of asymptomatic CE in most adults and children with DKA (13)(14)(15)(16). This age dependence may point to developmental changes in cerebral metabolism as critical elements in the pathogenesis of CE.…”

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confidence: 99%

Cerebral Edema in Childhood Diabetic Ketoacidosis

et al. 2004

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OBJECTIVE -Children who develop cerebral edema (CE) during diabetic ketoacidosis (DKA) exhibit definable signs and symptoms of neurological collapse early enough to allow intervention to prevent brain damage. Our objective was to develop a model for early detection of CE in children with DKA. RESEARCH DESIGN AND METHODS-A training sample of 26 occurrences of DKA complicated by severe CE and 69 episodes of uncomplicated DKA was reviewed. Signs of neurological disease were incorporated into a bedside evaluation protocol that was applied to an independent test sample of 17 patients previously reported to have developed symptomatic CE during treatment for DKA. Head computed tomograms and their reports were reviewed.RESULTS -The protocol allowed 92% sensitivity and 96% specificity for the recognition of CE sufficiently early for intervention. The diagnostic criteria were fulfilled in two temporal patterns, defining early-and late-onset CE. Although initial computed tomograms were often normal, the findings also included diffuse CE and focal brain injury, the latter only in patients with an early onset of abnormal neurological signs.CONCLUSIONS -CE may occur in the absence of acute changes on head computed tomograms. Early detection of CE at the bedside using an evidence-based protocol permits intervention in time to prevent permanent brain damage. Diabetes Care 27:1541-1546, 2004M ost children with diabetic ketoacidosis (DKA) exhibit abnormal neurological function. Therefore, evidence-based guidance for discerning the patients who require lifesaving intervention is needed. Cerebral dysfunction in DKA is usually a manifestation of metabolic derangement, but cerebral edema (CE) arises in ϳ1% of episodes and is a complication that frequently causes irreversible brain damage and death (1-7). Neurological collapse from CE is typically described as having sudden onset and progressing rapidly, with recovery depending on prompt reduction of intracranial pressure (4,8 -10). The object of this study was to delineate the signs and symptoms of neurological compromise that predict progression to severe CE in children with DKA.CE occurs rarely in patients older than age 20 years (8,11,12), despite the presence of asymptomatic CE in most adults and children with DKA (13-16). This age dependence may point to developmental changes in cerebral metabolism as critical elements in the pathogenesis of CE. For example, children's brains are reported to have higher fuel and oxygen requirements than those of adults (17,18). Hypoxia is further implicated because the brains of patients with DKA may extract blood oxygen less efficiently than healthy individuals (16) and the reported association of symptomatic CE with low partial pressures of carbon dioxide in arterial blood may reflect harmful cerebral vasoconstriction (5,6). Exuberant rehydration with hypotonic fluid and bicarbonate administration may aggravate the CE (5,6,9,11,12,19 -22); however, the evidence that CE is primarily iatrogenic is not compelling (6,8,(23)(24)(25)(26)(27)(28)(29)...

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Relation of Colloid Osmotic Pressure to Arterial Hypoxemia and Cerebral Edema During Crystalloid Volume Loading of Patients with Diabetic Ketoacidosis

Cited by 103 publications

References 27 publications

Prognostic factors in patients hospitalised with diabetic ketoacidosis at Kenyatta National Hospital, Nairobi

Prognostic factors in patients hospitalised with diabetic ketoacidosis at Kenyatta National Hospital, Nairobi

Management of Hyperglycemic Crises in Patients With Diabetes

Cerebral Edema in Childhood Diabetic Ketoacidosis

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