Skip to Main Content
Book cover for Oxford Handbook of Critical Care (3 edn) Oxford Handbook of Critical Care (3 edn)

A newer edition of this book is available.

Close

Contents

Book cover for Oxford Handbook of Critical Care (3 edn) Oxford Handbook of Critical Care (3 edn)
Disclaimer
Oxford University Press makes no representation, express or implied, that the drug dosages in this book are correct. Readers must therefore always … More Oxford University Press makes no representation, express or implied, that the drug dosages in this book are correct. Readers must therefore always check the product information and clinical procedures with the most up to date published product information and data sheets provided by the manufacturers and the most recent codes of conduct and safety regulations. The authors and the publishers do not accept responsibility or legal liability for any errors in the text or for the misuse or misapplication of material in this work. Except where otherwise stated, drug dosages and recommendations are for the non-pregnant adult who is not breastfeeding.

Balanced electrolyte: e.g. Ringer's lactate, Hartmann's solution.

Saline: e.g. 0.9% saline, 0.18% saline in 4% glucose.

Glucose: e.g. 5%, 10%, 20%, 50%.

Sodium bicarbonate: e.g. 1.26%, 8.4%.

Crystalloid fluids to provide daily requirements of water and electrolytes. They should be given to critically ill patients as a continuous background infusion to supplement fluids given during feeding or to carry drugs.

Higher concentration glucose infusions may be used to prevent hypoglycaemia.

Crystalloid fluids may contain potassum chloride supplements.

Sodium bicarbonate may be used to correct metabolic acidosis, for urinary alkalinisation, etc.

IV.

Significant plasma volume deficit should be replaced with colloid solutions since crystalloids are rapidly lost from the plasma, particularly during periods of increased capillary leak, e.g. sepsis.

As most plasma substitutes are carried in saline solutions, any additional salt containing crystalloid infusion is only needed to replace excess sodium losses.

The sodium content of 0.9% saline is equivalent to that of extracellular fluid. Therefore, salt‐containing solutions distribute throughout the extracellular fluid space.

Ringer's lactate or Hartmann's solution avoid hyperchloraemic acidosis caused by the relative excess chloride infused with 0.9% saline. Hyperchloraemic acidosis may adversely affect coagulation and renal function though human data are lacking.

A daily requirement of 70–80mmol sodium is normal although there may be excess loss in sweat and from the gastrointestinal tract. This can be provided as saline or balanced electrolyte solution.

5% glucose is used to supply intravenous water requirements. Since there are no electrolytes to favour distribution to one space or another, water distributes uniformly throughout the extracellular and intracellular spaces. The 50g/L glucose content ensures an isotonic solution, but only provides 200Cal/L. Normal requirement is approximately 1.5–2L/d.

Water loss in excess of electrolytes is uncommon but occurs in excess sweating, fever, hyperthyroidism, diabetes insipidus, and hypercalcaemia. 5% glucose is an appropriate replacement fluid for water loss.

Potassium chloride must be given slowly since rapid injection may cause fatal arrhythmias. No more than 40mmol/h should be given and even this may be dangerous in some patients. Up to20mmol/h is safer. The frequency of infusion is dictated by plasma potassium measurements.

Na+ K+ HCO3   Cl Ca2+

0.9% saline

150

150

Hartmann's

131

5

29

111

2

0.18% saline in 4% glucose

30

30

Na+ K+ HCO3   Cl Ca2+

0.9% saline

150

150

Hartmann's

131

5

29

111

2

0.18% saline in 4% glucose

30

30

H+ Na+ K+ HCO3   Cl

Gastric

40–60

20–80

5–20

150

100–150

Biliary

120–140

5–15

30–50

80–120

Pancreatic

120–140

5–15

70–110

40–80

Small bowel

120–140

5–15

20–40

90–130

Large bowel

100–120

5–15

20–40

90–130

H+ Na+ K+ HCO3   Cl

Gastric

40–60

20–80

5–20

150

100–150

Biliary

120–140

5–15

30–50

80–120

Pancreatic

120–140

5–15

70–110

40–80

Small bowel

120–140

5–15

20–40

90–130

Large bowel

100–120

5–15

20–40

90–130

Nutrition—use and indications, p126; Electrolytes (Na+, K+, Cl, HCO3  ), p212; Sodium bicarbonate, p244; Colloids, p246; Electrolyte management, p482; Hyponatraemia, p486; Hypokalaemia, p490; Metabolic acidosis, p504; Hypoglycaemia, p506.

Isotonic sodium bicarbonate 1.26%.

Hypertonic sodium bicarbonate 8.4%.

Correction of metabolic acidosis.

Alkalinisation of urine, e.g. for salicylate overdose, treatment of rhabdomyolysis.

Alkalinisation of blood, e.g. for treatment of tricyclic antidepressant overdose.

IV.

Isotonic (1.26%) sodium bicarbonate may be used to correct acidosis associated with renal failure or to induce a forced alkaline diuresis.

The hypertonic (8.4%) solution (1mEq HCO3  /mL) is rarely required in intensive care practice to raise blood pH in severe metabolic acidosis.

Bicarbonate therapy is inappropriate when tissue hypoperfusion or necrosis is present.

Administration may be indicated as either specific therapy (e.g. alkaline diuresis for salicylate overdose) or if the patient is dyspnoeic in the absence of tissue hypoperfusion (e.g. renal failure).

The PaCO2 may rise if minute volume is not increased.

Bicarbonate cannot cross the cell membrane without dissociation so the increase in PaCO2 may result in intracellular acidosis and depression of myocardial cell function.

A decrease in plasma ionised calcium as a result of alkalinisation may also cause a decrease in myocardial contractility. Significantly worse haemodynamic effects have been reported with bicarbonate compared to equimolar saline in patients with severe heart failure.

Convincing human data that bicarbonate improves myocardial contractility or increases responsiveness to circulating catecholamines in severe acidosis are lacking. Acidosis secondary to myocardial depression is related to intracellular changes that are not accurately reflected by arterial blood chemistry.

Excessive administration may cause hyperosmolality, hypernatraemia, hypokalaemia, and sodium overload.

Bicarbonate may decrease tissue oxygen availability by a left shift of the oxyhaemoglobin dissociation curve.

Sodium bicarbonate does have a place in the management of acid retention or alkali loss, e.g. chronic renal failure, renal tubular acidosis, fistulae, diarrhoea. Fluid and potassium deficit should be corrected first.

Na+ K+ HCO3   Cl Ca2+

1.26% sodium bicarbonate

150

150

8.4% sodium bicarbonate

1000

1000

Na+ K+ HCO3   Cl Ca2+

1.26% sodium bicarbonate

150

150

8.4% sodium bicarbonate

1000

1000

Blood gas analysis, p154; Electrolytes (Na+, K+, Cl, HCO3  ), p212; Electrolyte management, p482; Hypernatraemia, p484; Hypokalaemia, p490; Metabolic acidosis, p502.

Albumin: e.g. 4.5–5%, 20–25% human albumin solution.

Dextran: e.g. 6% Dextran 70.

Gelatin: e.g. 3.5% polygeline, 4% succinylated gelatin.

Hydroxyethyl starch: e.g. 6% hetastarch, 6% hexastarch, 6 and 10% pentastarch, 6% and 10% tetrastarch.

Replacement of plasma volume deficit.

Short‐term volume expansion (gelatin, dextran).

Medium‐term volume expansion (albumin, pentastarch, tetrastarch).

Long‐term volume expansion (hetastarch, hexastarch).

IV.

Dilution coagulopathy.

Anaphylaxis.

Interference with blood crossmatching (Dextran 70).

Nephropathy (high dose hydroxyethyl starches).

Smaller volumes of colloid are required for resuscitation with less contribution to oedema. Maintenance of plasma colloid osmotic pressure (COP) is a useful effect not seen with crystalloids, but colloids contain no clotting factors or other plasma enzyme systems.

Albumin is the main provider of COP in the plasma and has a number of other functions. There is no evidence that maintenance of plasma albumin levels, as opposed to maintenance of plasma COP with artificial plasma substitutes, is advantageous.

Hyperoncotic colloids can be used where salt restriction is necessary. This is rarely necessary as plasma volume expansion relates to weight of colloid infused rather than concentration. Artificial colloids used with ultrafiltration or diuresis are just as effective in oedema states.

Polygeline is a 3.5% solution and contains calcium (6.25mmol/L). The calcium content prevents the use of the same administration set for blood transfusions. Succinylated gelatin is a 4% solution and does not contain calcium.

Hydroxyethyl starch solutions are protected from metabolism due to a high degree of substitution (proportion of glucose units substituted with hydroxyethyl groups—DS) or a high C2:C6 ratio of carbon atoms substituted. Prolonged itching related to intradermal deposition, coagulopathy, and nephropathy are complications if excessive doses of higher molecular weight hydroxyethyl starches are used.

Pentastarch and tetrastarch provide only a short‐term volume expanding effects.

Hydroxyethyl starches in balanced electrolyte solutions are available. These avoid the problem of hyperchloraemic acidosis in higher doses. There is also some evidence of less coagulation disturbance.

Transport of various molecules.

Free radical scavenging.

Binding of toxins.

Inhibition of platelet aggregation.

Albumin

+++

Dextran 70

++

Succinylated gelatin

++

Polygeline

+

Hetastarch (high MW, high DS, low C2:C6 ratio)

++++

Hexastarch (medium MW, high DS, high C2:C6 ratio)

++++

Pentastarch (medium MW, low DS, low C2:C6 ratio)

++

Tetrastarch (low MW, low DS, high C2:C6 ratio)

++

Albumin

+++

Dextran 70

++

Succinylated gelatin

++

Polygeline

+

Hetastarch (high MW, high DS, low C2:C6 ratio)

++++

Hexastarch (medium MW, high DS, high C2:C6 ratio)

++++

Pentastarch (medium MW, low DS, low C2:C6 ratio)

++

Tetrastarch (low MW, low DS, high C2:C6 ratio)

++

Persistence is dependent on molecular size and protection from metabolism.

High DS and high C2:C6 ratio protect hydroxyethyl starch from metabolism.

All artificial colloids are polydisperse (i.e. there is a range of molecular sizes).

The SAFE Study Investigators. (2004) A comparison of albumin and saline for fluid resuscitation in the intensive care unit. N Engl J Med  350: 2247–56.
 
Brunkhorst F, Engel C, Bloos F, et al. (2008) Intensive insulin therapy and pentastarch resuscitation in severe sepsis. N Engl J Med  358: 125–39.

Colloid osmotic pressure, p238; Crystalloids, p242; Basic resuscitation, p338; Fluid challenge, p342; Anaphylactoid reactions, p578.

Blood cells are eventually destroyed by oxidant damage during storage of whole blood. Since white cells and plasma enzyme systems are important in this cellular destruction, effects are correspondingly less severe for packed red cells. Blood used for transfusion in most of Europe is now routinely leukodepleted to prevent acute non‐haemolytic transfusion reactions. Microaggregate formation is associated with platelets, white cells, and fibrin, and range in size from 20–170µm. The risk of microaggregate damage is reduced with packed cells. In addition to spherocytosis and haemolysis, prolonged storage depletes ATP and 2,3‐DPG levels, thus increasing the O2 affinity of the red cells. If whole blood is to be used in critically ill patients, it should be as fresh as possible.

In an emergency with massive blood loss that threatens life, it is permissible to transfuse O‐negative packed cells, but a sample must be taken for grouping prior to transfusion. With modern laboratory procedures, it is possible to obtain ABO compatibility for group specific transfusion within 5–10min and a full crossmatch in 30min.

Citrate toxicity—hypocalcaemia is rarely a problem. The prophylactic use of calcium supplementation is not recommended.

Potassium load—potassium returns to cells rapidly, but hyperkalaemia may be a problem if blood is stored at room temperature.

Jaundice—haemolysis of incompatible or old blood.

Pyrexia—immunological transfusion reactions to incompatible red or white cells or platelets or blood products

DIC—partial activation of clotting factors and destruction of stored cells, either in old blood or when transfusion is incompatible.

Anaphylactoid reaction—urticaria is common and probably due to a reaction to transfused plasma proteins; if severe, it may be treated by slowing the transfusion and giving chlorpheniramine 10mg IV/IM. In severe anaphylaxis, in addition to standard treatment, the transfusion should be stopped and saved for later analysis. A sample should be taken for further crossmatching.

Transmission of disease—including viruses, parasites (malaria), prions.

Transfusion‐related acute lung injury (TRALI) and other immune reactions.

A multicentre trial suggested liberal transfusion in the critically ill produced less favourable outcomes, particularly in younger, less sick patients, than using a trigger haemoglobin of 7g/dL. This was performed with non‐leukodepleted blood; the validity with leukodepleted blood now in common use is uncertain.

Hebert P, Wells G, Blajchman M, et al. for the Tranfusion Requirements in Critical Care Investigators. (1999) A multicentre, randomised, controlled clinical trial of transfusion requirements in critical care. N Engl J Med  340: 409–17.

Basic resuscitation, p338; Upper gastrointestinal haemorrhage, p412; Bleeding varices, p414; Lower intestinal bleeding and colitis, p420; Jaundice, p428; Anaemia, p472; Sickle cell disease, p474; Haemolysis, p476; Hyperkalaemia, p488; Anaphylactoid reactions, p578.

Plasma, e.g. fresh frozen plasma.

Platelets.

Concentrates of coagulation factors, e.g. cryoprecipitate, factor VIII concentrate, factor IX complex, Octaplex.

Recombinant technologies, e.g. factor VIIa, factor VIII.

Vitamin K deficiency (fresh frozen plasma, factor IX complex, Octaplex).

Haemophilia (cryoprecipitate, factor VIII, recombinant factor VIIa).

von Willebrand's disease (cryoprecipitate).

Fibrinogen deficiency (cryoprecipitate).

Christmas disease (factor IX complex).

IV.

A unit (150mL) of fresh frozen plasma is usually collected from one donor and contains all coagulation factors, including 200U factor VIII, 200U factor IX, and 400mg fibrinogen. It is stored at –30°C and should be infused within 2h once defrosted.

Platelet concentrates are viable for three days when stored at room temperature. Viability decreases if they are refrigerated. They must be infused quickly via a short giving set with no filter.

Indications for platelet concentrates include platelet count <10×109 or <50×109 with spontaneous bleeding or to cover invasive procedures and spontaneous bleeding with platelet dysfunction. They are less useful in conditions associated with immune platelet destruction (e.g. ITP).

A 15mL vial of cryoprecipitate contains 100U factor VIII, 250mg fibrinogen, factor XIII, and von Willebrand factor and is stored at –30°C.

In haemophilia, cryoprecipitate is given to achieve a factor VIII level >30% of normal.

Factor VIII concentrate contains 300U factor VIII per vial. In severe haemorrhage due to haemophilia, 10–15U/kg are given 12‐hourly.

Recombinant factor VIIa is indicated for control of bleeding in patients with haemophilia with inhibitors to factors VIII or IX, or congenital factor VII deficiency. It forms complexes with exposed tissue factor and is not dependent on the presence of factors VIII or IX. It has been shown to reduce blood transfusion requirements in major blunt trauma. Success has been reported in cases of uncontrollable intra‐operative bleeding (90mcg/kg repeated every 2–3h until bleeding stops).

Octaplex is a prothrombin complex concentrate for the substitution of factors II, VII, IX, and X in treatment or prophylaxis of hereditary and acquired coagulation factor disorders, e.g. warfarin overdose.

Boffard KD, for the NovoSeven Trauma Study Group. (2005) Recombinant factor VIIa as adjunctive therapy for bleeding control in severely injured trauma patients: two parallel randomised, placebo‐controlled, double‐blind clinical trials. J Trauma  59: 8–15.

Plasma exchange, p114; Full blood count, p220; Coagulation monitoring, p222; Colloids, p246; Blood transfusion, p248; Anticoagulants, p318; Bleeding disorders, p468; Clotting disorders, p470; Platelet disorders, p478.

Close
This Feature Is Available To Subscribers Only

Sign In or Create an Account

Close

This PDF is available to Subscribers Only

View Article Abstract & Purchase Options

For full access to this pdf, sign in to an existing account, or purchase an annual subscription.

Close