Blogging has slowed a bit as I’ve been travelling to the UK and am running courses here all week.
Just in case you’re desperate to read something useful, I came across a guideline on The Management of Diabetic Ketoacidosis in Adults by the Joint British Diabetes Societies Inpatient Care Group
The guideline contain the following approaches:
Measurement of blood ketones, venous (not arterial) pH and bicarbonate and their use as treatment markers
Monitoring of ketones and glucose using bedside meters when available and operating within their quality assurance range
Use of venous blood rather than arterial blood in blood gas analysers
Monitoring of electrolytes on the blood gas analyser with intermittent laboratory confirmation
Continuation of long acting insulin analogues (Lantus® or Levemir®) as normal
Involvement diabetes specialist team as soon as possible
There is also a section on ‘Controversial Areas’, discussing such issues as bicarbonate therapy, rate of fluid therapy, and even 0.9% saline versus Hartmann’s (Ringer’s Lactate) solution, although this part was desperately disappointing, with the following bizarre excuse given for not recommending the latter:
“In theory replacement with glucose and compound sodium lactate (Hartmann’s solution) with potassium, would prevent hyperchloraemic metabolic acidosis, as well as allow appropriate potassium replacement. However, at present this is not readily available as a licensed infusion fluid.”
Apart from that, this appears to be an interesting and potentially useful document. The Management of Diabetic Ketoacidosis in Adults Joint British Diabetes Societies Inpatient Care Group
Working out the expected compensatory response to an acid base disturbance often reveals a second acid-base problem that was otherwise hidden. I regularly use Winter’s formula when I see a metabolic acidosis, but I have trouble remembering the others, so here they are, from Harwood-Nuss’ Clinical Practice of Emergency Medicine (apologies if you ‘think’ in kilopascals): Formulas Describing Expected Compensatory Response to Primary Acid–Base Disturbances Simple Metabolic Acidosis
Predicted decreased PCO2 mm Hg = 1.2 × Δ(HCO3-) mEq/L
Predicted PCO2 mm Hg = 1.5(HCO3-) mEq/L + 8 ± 2
Anticipated PCO2 approximates last two digits of arterial pH
A multinational European working group produced the following evidence-based recommendations for preventing acute kidney injury (AKI). Read the full guideline before criticising – some are just suggestions, some recommendations; I have not included the strength of recommendation or grade of evidence in my summary below. Volume expansion
Controlled fluid resuscitation in true or suspected volume depletion
There is little evidence-based support for the preferential use of crystalloids or colloids
Avoid 10% HES 250/0.5 as well as higher-molecular-weight preparations of HES and dextrans in sepsis
Prophylactic volume expansion by isotonic crystalloids in patients at risk of contrast nephropathy. Use isotonic sodium bicarbonate solution, especially for emergency procedures
Prophylactic volume expansion with crystalloids to prevent AKI by certain drugs (amphotericin B, antivirals including foscarnet, cidofovir, and adefovir, as well as drugs causing crystal nephropathy such as indinavir, acyclovir, and sulfadiazine)
Diuretics
Do not use loop diuretics to prevent or ameliorate AKI
Vasopressors and inotropes
Maintain mean arterial pressure (MAP) at least 60–65 mmHg, however, target pressure should be individualized where possible, especially if knowledge of the premorbid blood pressure is available.
In case of vasoplegic hypotension as a result of sepsis or SIRS use either norepinephrine or dopamine (along with fluid resuscitation) as the first-choice vasopressor agent to correct hypotension.
Do not use low-dose dopamine for protection against AKI.
Vasodilators
Use vasodilators for renal protection when volume status is corrected and the patient is closely hemodynamically monitored with particular regard to the development of hypotension.
Prophylactic use of fenoldopam, if available, in cardiovascular surgery patients at risk of AKI. Do not use fenoldopam for prophylaxis of contrast nephropathy.
Use theophylline to minimize risk of contrast nephropathy, especially in acute interventions when hydration is not feasible.
Do not use natriuretic peptides as protective agents against AKI in critically ill patients, while its use may be considered during cardiovascular surgery.
Hormonal manipulation and activated protein C
Avoid routine use of tight glycemic control in the general ICU population. Use “Normal for age’’ glycemic control with intravenous (IV) insulin therapy to prevent AKI in surgical ICU patients, on condition that it can be done adequately and safely applying a local protocol which has proven efficacy in minimizing rate of hypoglycemia.
Do not use thyroxine, erythropoietin, activated protein C or steroids routinely to prevent AKI.
Metabolic interventions
All patients at risk of AKI should have adequate nutritional support, preferably through the enteral route
Do not use N-acetylcysteine as prophylaxis against contrast induced nephropathy or other forms AKI in critically ill patients because of conflicting results, possible adverse reactions, and better alternatives.
Do not routinely use selenium to protect against renal injury.
Extracorporeal therapies
Use periprocedural continuous veno-venous hemofiltration (CVVH) in an ICU environment to limit contrast nephropathy after coronary interventions in high-risk patients with advanced chronic renal insufficiency
Prevention of acute kidney injury and protection of renal function in the intensive care unit
Expert opinion of the working group for nephrology, ESICM Intensive Care Med. 2010 Mar;36(3):392-411
Previous work in severe sepsis/septic shock patients has shown that a decrease in lactate concentration by at least 10% during emergency department resuscitation predicts survival. Since this is a potential alternative resuscitation goal to a central venous oxygen saturation (ScvO2) of 70% (as per surviving sepsis campaign guidelines), lactate clearance was compared with ScvO2 in a randomised non-inferiority trial of 300 patients.
All patients were managed in the ED and received fluids, antibiotics, and vasopressors as needed. Then lactate clearance or ScvO2 were measured, and if the respective goals of 10% or 70% were not met, packed cells or dobutamine were given depending on haematocrit. Lactate clearance was the percentage decrease in lactate between two venous specimens taken two hours apart.
Interestingly only 29 patients received either packed cells or dobutamine. Each group was similar in terms of time to antibiotic therapy and amount of fluid given. Patients in the group resuscitated to a lactate clearance of 10% or higher had 6% lower in-hospital mortality than those resuscitated to an ScvO2 of at least 70% (95% CI for this difference, –3% to 15%) exceeding the –10% predefined noninferiority threshold.
The authors conclude ‘these data support the substitution of lactate measurements in peripheral venous blood as a safe and efficacious alternative to a computerized spectrophotometric catheter in the resuscitation of sepsis.’ Lactate clearance vs central venous oxygen saturation as goals of early sepsis therapy: a randomized clinical trial JAMA. 2010 Feb 24;303(8):739-46
A high serum lactate does not necessarily mean a bad prognosis: it all depends on the cause.
I made this diagram as a mnemonic for the causes of high lactates:
Additional information added 1st June 2011: One cause of an elevated lactate may be artefactual, secondary to interference with the assay (used on ABG machines) by ethylene glycol. The assay may also be subject to interference from certain drugs at toxic levels such as isoniazid, acetaminophen and thiocyanate. This information is from the Renal Fellow Network.
Ionised hypocalcaemia has been observed post-cardiac arrest in previous studies. Investigators in Utah induced VF in a swine model and resuscitated them back to spontaneous circulation1. Ionised hypocalcaemia was associated with hypotension and impaired LV function, and its treatment with a calcium infusion resulted in improved mean arterial pressure and left ventricular stroke work.
Although iv calcium is not recommended as a blind treatment in cardiac arrest, in part due to concerns about exacerbating cellular injury, this study reminds us that the treatment of ionised hypocalcaemia is important, and may be necessary after ROSC.
1. Hypocalcemia following resuscitation from cardiac arrest revisited Resuscitation 2010 Jan;81:117–122
A comprehensive summary of the literature presented by Professor Anne-Maree Kelly in June 2009 at 4ème SYMPOSIUM INTERNATIONAL BLOOD GASES AND CRITICAL CARE TESTING in France can be viewed on her presentation slides at the link below.
She summarises:
pH – Close enough agreement for clinical purposes in DKA, isolated metabolic disease; more work needed in shock, mixed disease
Bicarbonate – Close enough agreement for clinical purposes in most cases; more work needed in shock, mixed disease, calculated vs measured gap
pCO2 – NOT enough agreement for clinical purposes; potential as a screening test
Potassium – Insufficient agreement between serum and BG values for clinical purposes
