Haematology
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Question 10 of 300
You are managing a 22 year old patient who is receiving a blood transfusion following a road traffic collision in which he was knocked off his motorbike. Within 5 minutes of starting the blood transfusion, the patient is complaining of pain at the site of the IV line and feeling flushed and unwell. His observations show that he is tachycardic (125 bpm) and pyrexial (39.1°C). Which of the following is the most likely explanation?
Answer:
The most serious reactions are caused by transfusion of ABO-incompatible red cells which react with the patient’s anti-A or anti-B antibodies. There is rapid destruction of the transfused red cells in the circulation (intravascular haemolysis) and the release of inflammatory cytokines. The patient often quickly becomes shocked and may develop acute renal failure and disseminated intravascular coagulation (DIC). Conscious patients often become very unwell within the first few minutes of transfusion, complaining of flushing, loin and abdominal pain and ‘a feeling of impending doom’. If the patient is unconscious, anaesthetised or cannot communicate, the first indication of a reaction may be tachycardia, hypotension and bleeding into the skin or from needle wounds. Febrile non-haemolytic transfusion reaction (FNHTR)s are characterised by fever, usually accompanied by chills, in the absence of other systemic symptoms.Transfusion Reactions
Haematology
Last Updated: 14th December 2023
Blood products
- Blood components
- Red cells
- Red cells are used to restore oxygen carrying capacity in patients with anaemia or blood loss where alternative treatments are ineffective or inappropriate.
- Platelets
- Platelet transfusion is indicated for the treatment or prevention of bleeding in patients with a low platelet count (thrombocytopenia) or platelet dysfunction.
- Fresh frozen plasma (FFP)
- Plasma is frozen soon after collection to maintain the activity of blood-clotting factors. FFP is indicated for the treatment of patients with bleeding due to multiple clotting factor deficiencies such as disseminated intravascular coagulation (DIC). It may also be used in patients with inherited clotting factor deficiencies (e.g. Factor V deficiency) where a clotting factor concentrate is not yet available.
- Cryoprecipitate
- Cryoprecipitate is made by thawing UK donor FFP at 4°C, producing a cryoglobulin rich in fibrinogen, Factor VIII and von Willebrand factor. It was developed as a treatment for haemophilia but this use has now been replaced by Factor VIII concentrate. Cryoprecipitate is mainly used as a more concentrated, hence lower volume for infusion, source of fibrinogen than FFP.
- Red cells
- Plasma derivatives
- Human albumin solution
- The clinical indications for HAS are controversial. Indications may include initiating diuresis in hypoalbuminaemic patients with liver cirrhosis or nephrotic syndrome, removal of large volumes of ascites in patients with portal hypertension and to assist the reduction of high bilirubin levels by exchange transfusion in the newborn (unconjugated bilirubin binds to albumin). Crystalloid solutions or synthetic colloidal plasma substitutes are alternatives for use as plasma expanders in acute blood or plasma loss. HAS should not be used to ‘correct’ the low serum albumin level often associated with acute or chronic illness.
- Clotting factor concentrates
- Single-factor concentrates are available for the treatment of most inherited coagulation deficiencies except Factor V and Factor II (prothrombin). Most patients in the UK with severe haemophilia A are now treated with recombinant Factor VIIIc, which carries no risk of viral or prion transmission.
- Fibrinogen concentrate (Factor I) is, at present, only licensed in the UK for the treatment of congenital hypofibrinogenaemia but there is encouraging international experience of its effectiveness in the much more common setting of acquired hypofibrinogenaemia (e.g. DIC, traumatic haemorrhage, massive transfusion). Many coagulation experts believe that it will replace the use of cryoprecipitate for this purpose in view of its ease of administration, convenience of storage and standardised fibrinogen content.
- Prothrombin complex concentrate (PCC) contains Factors II, VII, IX and X. It has replaced FFP as the recommended treatment for rapid reversal of warfarin overdose, with elevated international normalised ratio (INR) and severe bleeding, in view of its superior efficacy, ease of administration and lower risk of severe allergic reactions or fluid overload. Modern formulations of PCC do not contain activated clotting factors and have a low risk of causing thrombotic complications. PCC may also be used to treat bleeding due to the coagulopathy associated with liver disease.
- Immunoglobulin solutions
- Normal immunoglobulin: contains antibodies to viruses that are common in the population. Intramuscular normal immunoglobulin may be used to protect susceptible contacts against hepatitis A, measles or rubella. High-dose intravenous immunoglobulin is used as replacement therapy in patients with severe immunoglobulin deficiency and in the treatment of autoimmune diseases such as idiopathic thrombocytopenic purpura (ITP).
- Specific immunoglobulins: made from selected donors with high antibody levels to the target of treatment. Examples include tetanus, hepatitis B and rabies immunoglobulins as well as anti-D immunoglobulin for the prevention of maternal sensitisation to RhD in pregnancy.
- Human albumin solution
Blood group pathophysiology
Blood group antigens are molecules present on the surface of red blood cells. The main blood group systems are the ABO system and the Rh system. Blood group antibodies are usually produced when an individual is exposed to blood of a different group by transfusion or pregnancy (‘alloantibodies’). This is a particular problem in patients who require repeated transfusions, and can cause difficulties in providing fully compatible blood if the patient is immunised to several different groups. Antibodies to ABO antigens are naturally occurring and are found in everyone after the first 3 months of life.
ABO System:
- There are four main blood groups: A, B, AB and O. All normal individuals have antibodies to the A or B antigens that are not present on their own red cells.
- Blood group O is the most common in the UK (47 %), followed by group A (42 %), group B (8 %) and finally group AB (3 %).
- Individuals of blood group O are sometimes known as universal donors as their red cells have no A or B antigens. However, their plasma does contain anti-A and anti-B that, if present in high titre, has the potential to haemolyse the red cells of certain non-group O recipients.
- ABO-incompatible red cell transfusion is often fatal and its prevention is the most important step in clinical transfusion practice. Anti-A and/or anti-B in the recipient’s plasma binds to the transfused cells and activates the complement pathway, leading to destruction of the transfused red cells (intravascular haemolysis) and the release of inflammatory cytokines that can cause shock, renal failure and disseminated intravascular coagulation (DIC). The accidental transfusion of ABO-incompatible blood is now classified as a ‘never event’ by the UK Departments of Health.
Blood Groups. (Image by OpenStax College [CC BY 3.0 , via Wikimedia Commons)
- There are five main Rh antigens on red cells for which individuals can be positive or negative: C/c, D and E/e. RhD is the most important in clinical practice. Around 85% of white Northern Europeans are RhD positive, rising to virtually 100% of people of Chinese origin.
- Antibodies to RhD (anti-D) are only present in RhD negative individuals who have been transfused with RhD positive red cells or in RhD negative women who have been pregnant with an RhD positive baby. IgG anti-D antibodies can cause acute or delayed haemolytic transfusion reactions when RhD positive red cells are transfused and may cause haemolytic disease of the fetus and newborn. It is important to avoid exposing RhD negative girls and women of childbearing potential to RhD positive red cell transfusions except in extreme emergencies when no other group is immediately available.
Other significant blood group systems:
- Alloantibodies to the Kidd (Jk) system are an important cause of delayed haemolytic transfusion reactions.
- Kell (anti-K) alloantibodies can cause HDFN and it is important to avoid transfusing K positive red cells to K negative girls and women of childbearing potential.
Acute transfusion reactions (ATRs)
Less severe reactions:
- Febrile non-haemolytic transfusion reactions (FNHTRs)
- FNHTR are characterised by fever, sometimes accompanied by shivering, muscle pain and nausea. These are much less common since leucodepleted blood components were introduced. They can occur up to 2 hours after completion of the transfusion and are more common in multi-transfused patients receiving red cells.
- Mild FNHTRs (pyrexia >38°C, but <2°C rise from baseline) can often be managed simply by slowing (or temporarily stopping) the transfusion. Giving an antipyretic, such as paracetamol, may be helpful. The patient should be monitored closely in case these are the early signs of a more severe ATR.
- In the case of moderate FNHTRs (pyrexia >2°C above baseline or >39°C or rigors and/or myalgia), the transfusion should be stopped. If the symptoms worsen, or do not quickly resolve, consider the possibility of a haemolytic or bacterial reaction. In most cases it is prudent to resume transfusion with a different blood unit.
- Mild allergic transfusion reactions
- Symptoms are confined to itching (pruritus) and/or skin rash (hives) with no change in vital signs. They are most common in patients receiving plasma-rich components such as FFP or platelets.
- Symptoms often improve if the transfusion is slowed and an antihistamine (e.g. chlorpheniramine) is administered orally or intravenously. The patient must be monitored closely for development of a more severe reaction, in which case the transfusion must be stopped.
Severe and life-threatening reactions:
- Acute haemolytic transfusion reactions
- The most serious reactions are caused by transfusion of ABO-incompatible red cells which react with the patient’s anti-A or anti-B antibodies. There is rapid destruction of the transfused red cells in the circulation (intravascular haemolysis) and the release of inflammatory cytokines. The patient often quickly becomes shocked and may develop acute renal failure and disseminated intravascular coagulation (DIC).
- ABO-incompatible transfusion is usually caused by human error when taking or labelling pre-transfusion blood samples, collecting components from the blood bank or satellite refrigerator and/or failing to perform a correct identity check of blood pack and patient at the bedside. If red cells are transfused to the wrong patient, there is around a 30% chance they will be ABO incompatible. Major morbidity (requiring intensive care or renal dialysis) occurs in up to 30% of cases and 5–10% of episodes contribute to the death of the patient.
- Conscious patients often become very unwell within the first few minutes of transfusion, complaining of flushing, loin and abdominal pain and ‘a feeling of impending doom’. If the patient is unconscious, anaesthetised or cannot communicate, the first indication of a reaction may be tachycardia, hypotension and bleeding into the skin or from needle wounds.
- Management includes:
- Maintain venous access with physiological saline and call for urgent medical support.
- Check the compatibility label on the blood pack against the patient’s ID band (and seek confirmation of identity from the patient, parent or carer if possible).
- Inform the transfusion laboratory urgently. If the wrong blood has been transfused, another patient may be at risk. Return the (sealed) transfusion pack and giving-set for investigation.
- Seek early support and advice from critical care and haematology teams and admit the patient to an intensive care unit if possible.
- Severe allergic or anaphylactic reactions
- Shock or severe hypotension associated with wheeze (bronchospasm), stridor from laryngeal oedema or swelling of face, limbs or mucous membranes (angioedema) is strongly suggestive of anaphylaxis – an acute, life-threatening emergency. Other skin changes may include flushing and urticaria (‘nettle rash’ or hives) that also occur in less severe allergic reactions. Severe allergic and anaphylactic reactions may occur with all blood components but are most commonly reported with plasma-rich components such as platelets or FFP.
- Management includes:
- UK Resuscitation Council (UKRC) guidelines recommend the urgent administration of intramuscular (IM) epinephrine to treat anaphylaxis (adult dose 0.5 mL of 1:1000 (500 µg)). The IM route is rapidly effective (and life-saving) and prevents delay in attempting to obtain venous access in a shocked patient. It is not contraindicated in patients with coagulopathy or low platelet count.
- Urgent expert medical care should be called immediately (e.g. critical care outreach team or local equivalent).
- After initial resuscitation, parenteral steroids or antihistamines may be given but these should not be the first-line therapy.
- Bacterial contamination of blood unit
- Blood components may be contaminated by bacteria, most often derived from the donor arm at the time of collection, which can proliferate on storage and harm the recipient. Bacteria from the normal skin flora, such as the coagulase negative staphylococci rarely produce severe infections although febrile reactions may occur. More pathogenic gram positive bacteria, such as Staphylococcus aureus, and gram negatives, such as E. coli, Klebsiella spp. and Pseudomonas spp., may produce life-threatening reactions. Although rare, this more often occurs with platelet components (which are stored at 22–24°C) than with red cells refrigerated at 2–6°C and can rapidly be fatal. The risk increases with storage time after donation and is the main reason for the short shelf life of platelet components.
- The transfusion of a pack contaminated with highly pathogenic bacteria often causes an acute severe reaction soon after the transfusion is started. Initially, this may be indistinguishable from an acute haemolytic reaction or severe allergic reaction. Typical symptoms and signs include rigors, fever (usually >2°C above baseline), hypotension and rapidly developing shock and impaired consciousness.
- Management includes:
- Inspection of the pack may show abnormal discoloration, aggregates or offensive smell, but many packs appear normal.
- Blood cultures should be taken from the patient and treatment immediately started with an intravenous broad spectrum antibiotic combination covering gram negative and gram positive bacteria (the local empirical antibiotic regimen used in patients with neutropenic sepsis is appropriate).
- Implicated components must be sealed to avoid leakage or contamination and returned to the transfusion laboratory for further investigation.
- The blood transfusion centre must be contacted immediately so that any associated components from the implicated donation can be urgently identified and withdrawn from hospital blood banks.
- Transfusion-related acute lung injury (TRALI)
- Classical TRALI is caused by antibodies in the donor blood reacting with the patient’s neutrophils, monocytes or pulmonary endothelium. Inflammatory cells are sequestered in the lungs, causing leakage of plasma into the alveolar spaces (non-cardiogenic pulmonary oedema).
- Most cases present within 2 hours of transfusion (maximum 6 hours) with severe breathlessness and cough productive of frothy pink sputum. It is often associated with hypotension (due to loss of plasma volume), fever and rigors and transient peripheral blood neutropenia or monocytopenia. Chest X-ray shows bilateral nodular shadowing in the lung fields with normal heart size. TRALI is often confused with acute heart failure due to circulatory overload and treatment with powerful diuretics may increase mortality.
- Treatment is supportive, with high-concentration oxygen therapy and ventilatory support if required. Steroid therapy is not effective. Managed appropriately, often with intensive care, there is now a high rate of survival and most patients recover within 1 to 3 days without long-term problems.
- Transfusion-associated circulatory overload (TACO)
- TACO is defined as acute or worsening pulmonary oedema within 6 hours of transfusion. Typical features include acute respiratory distress, tachycardia, raised blood pressure and evidence of positive fluid balance. It has probably been significantly under-reported in the past and may now be the most common cause of transfusion-related death in developed countries. Elderly patients are at particular risk and predisposing medical conditions include heart failure, renal impairment, low albumin concentration and fluid overload. Small patients, such as the frail elderly and children, are at increased risk of receiving inappropriately high-volume and rapid blood transfusions. Most reported cases involve red cell transfusions but high-volume FFP transfusions, sometimes given inappropriately for reversal of warfarin, have been identified as a risk. Poor pre-transfusion clinical assessment and inadequate monitoring during transfusion is a common feature of reported cases.
- The treatment of TACO involves stopping the transfusion and administering oxygen and diuretic therapy with careful monitoring and critical care support if required. The risk of TACO is reduced by careful consideration of the need to transfuse, clinical assessment for predisposing factors, prescription of appropriate volume and flow rate, and adequate monitoring during the procedure. The common assumption that one unit of red cells produces a rise in Hb of 10 g/L only applies to patients of 70–80 kg. A dose of 4 mL/kg will produce a rise of about 10 g/L. The use of single-unit transfusions in small, frail adults or prescription in millilitres (as in paediatric practice) has been recommended.
- Hypotensive reactions
- Hypotensive reactions are indicated by an isolated fall in systolic blood pressure of 30 mm Hg or more (to <80 mm Hg) during, or within one hour of, transfusion with no evidence of an allergic reaction or haemorrhage. Most are transient but they occasionally progress to shock and organ dysfunction. The cause of most of these reactions is unknown, although they may be more common in patients taking ACE inhibitors.
- Management involves stopping the transfusion and nursing the patient flat with leg elevation (or in the ‘recovery position’ if consciousness is impaired). Other causes of severe ATR should be excluded by clinical and laboratory investigation.
- Note: If a patient being transfused for haemorrhage develops hypotension, careful clinical assessment is essential as this may be due to continuing blood loss and continuation of the transfusion may be life-saving.
Delayed transfusion reactions (DTRs)
- Delayed haemolytic transfusion reactions (DHTRs)
- DHTRs occur more than 24 hours after transfusion in a patient who has previously been ‘alloimmunised’ to a red cell antigen by blood transfusion or pregnancy. The antibody may have fallen to a level that is undetectable by the pre-transfusion antibody screen and the patient is then inadvertently re-exposed to red cells of the immunising group. Antibodies to the Kidd (Jk) blood group system are the most common cause of DHTRs, followed by antibodies to Rh antigens.
- Transfusion of antigen-positive red cells causes a boost in the patient’s antibody levels (secondary immune response) leading to haemolysis of the transfused cells. Haemolysis becomes clinically apparent up to 14 days after the transfusion and signs may include a falling Hb concentration or failure to achieve the expected increment, jaundice, fever and occasionally haemoglobinuria or acute renal failure. Delayed reactions may be missed, especially if the patient has been discharged.
- Clinical suspicion of DHTRs should be confirmed by laboratory investigations including blood count and reticulocytes, examination of the blood film, plasma bilirubin, renal function tests and LDH. Serological investigations should include repeat blood group and antibody screen (on pre- and post-transfusion patient samples), DAT and elution of antibodies from the patient’s red cells for identification.
- Treatment of DHTRs is usually supportive, sometimes requiring further transfusion.
- Transfusion-associated graft-versus-host disease (TA-GvHD)
- This rare and almost always fatal complication occurs when viable lymphocytes in a blood donation engraft in the patient and mount an immune response against the recipient’s cells of a different HLA type. At-risk patients usually have impaired cell-mediated immunity and are unable to reject the foreign cells.
- Symptoms classically occur 7 to 14 days (maximum 30 days) after transfusion with fever, skin rash, diarrhoea, disturbed liver function and worsening bone marrow aplasia. Diagnosis is based on showing the typical features of acute GvHD in biopsies of affected organs and demonstration of donor-derived cells or DNA in the patient’s blood or tissues.
- Post-transfusion purpura (PTP)
- Affected individuals develop a very low platelet count and bleeding 5 to 12 days after transfusion of red cells. The typical patient is a parous female who is negative for a common platelet antigen, most commonly HPA-1a, and may have been initially sensitised by carrying a HPA-1a positive fetus in pregnancy. PTP is caused by re-stimulation of platelet-specific alloantibodies in the patient that also damage their own (antigen-negative) platelets by an ‘innocent bystander’ reaction. This severe, and potentially fatal, complication has become rare since the introduction of leucodepleted blood components.
- Advice in diagnosis and management should be sought from transfusion medicine specialists and Blood Service laboratories. Platelet transfusions are usually ineffective (but may be given in high doses in patients with life-threatening bleeding) but most patients show a prompt and sustained response to high-dose intravenous immunoglobulin (IVIg).
Transfusion-transmitted infections (TTIs)
Historically, transfusion-transmitted infections (TTIs) dominated the transfusion safety agenda but they are now rare in developed countries. However, constant vigilance is required to counter the risk from established and newly emergent pathogens in the era of mass international travel. Novel transfusion-transmissible agents, such as prions, have also emerged to threaten the safety of the blood supply.
- Viral infection
- Hepatitis A
- Hepatitis B
- Hepatitis C
- Hepatitis E
- Human immunodeficiency virus (HIV) 1 and 2
- Cytomegalovirus (CMV)
- Human T-cell lymphotropic virus types I and II (HTLV I and II)
- Human parvovirus B19 (HPV B19)
- West Nile Virus (WNV)
- Bacterial infection
- Syphilis
- Other bacterial infections (see above)
- Protozoal infections
- Malaria
- Chagas disease
Algorithm for management of acute transfusion reactions
Early recognition of ATRs by careful monitoring of vital signs during transfusion is important; especially the 15-minute checks. Patients should be asked to report symptoms that arise during the transfusion and for at least the next 24 hours.
- Patient exhibiting possible features of acute transfusion reaction (fever, chills, rigors, tachycardia, hyper- or hypotension, collapse, flushing, urticaria, pain (bone, muscle, chest, abdo), respiratory distress, nausea, malaise)
- Stop the transfusion
- Undertake rapid clinical assessment looking for ABC problems
- Check patient ID/blood compatibility level
- Visually assess unit for abnormal clumps or discolouration
- Patients with mild features (temp ≥ 38°C or rise of 1-2°C and/or pruritus/rash only)
- Continue transfusion
- Consider symptomatic treatment
- Monitor patient more frequently
- If symptoms/signs worsen, manage as for mod/severe reaction
- Patients with moderate features (temp ≥ 39°C or rise ≥ 2°C and/or other symptoms apart from pruritus/rash only)
- Monitor patient more frequently
- Consider bacterial contamination if the temp rises as above and review patient's underlying condition and transfusion history
- If consistent with underlying condition or transfusion history, consider continuation of transfusion at slower rate and appropriate symptomatic treatment
- If not consistent with condition or history, discontinue transfusion and perform appropriate investigations
- Patient with severe/life-threatening features (ABC problems/wrong blood given/evidence of contaminated unit)
- Call for urgent medical help
- Initiate resuscitation ABC
- If haemorrhage is not likely to be causing hypotension, discontinue transfusion
- Maintain venous access
- Monitor patient more frequently e.g. TPR, BP, SpO2, urinary output
- If likely anaphylaxis/severe allergy, follow anaphylaxis pathway
- If likely bacterial contamination, follow infection/sepsis pathway
- Use vital signs to guide intravenous physiological saline administration
- Inform hospital transfusion department
- Return unit (with administration set) to transfusion laboratory
- If bacterial contamination suspected, contact blood services to discuss recall of associated components
- Perform appropriate investigations
Investigations for acute transfusion reactions
- Fever (>2°C rise or >39°C) and/or chills, rigors, myalgia, nausea or vomiting and/or loin pain:
- Standard investigations (full blood count, renal and liver function tests, assessment of urine for Hb)
- Samples for repeat compatibility testing, direct antiglobulin test (DAT), lactate dehydrogenase (LDH) and haptoglobins
- Blood cultures
- Coagulation screen
- Angioedema
- Standard investigations
- Measure IgA level – if <0.07 g/L (in absence of generalised hypogammaglobulinaemia) perform confirmatory test with sensitive method and check for IgA antibodies
- Dyspnoea, wheeze or features of anaphylaxis
- Standard investigations
- Check O2 saturation or blood gases
- Chest X-ray (mandatory if symptoms severe)
- If severe or moderate allergic reaction suspected, measure IgA level (as above)
- If severe allergic/anaphylactic reaction, consider measurement of serial mast cell tryptase (immediate, 3 and 24 hours)
- Hypotension (isolated fall in systolic blood pressure of >30 mm Hg resulting in a level <80 mm Hg)
- Standard investigations plus investigations as for fever
- If allergic reaction suspected measure IgA level
- If severe allergic/anaphylactic reaction suspected, consider measurement of serial mast cell tryptase
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- Biochemistry
- Blood Gases
- Haematology
| Biochemistry | Normal Value |
|---|---|
| Sodium | 135 – 145 mmol/l |
| Potassium | 3.0 – 4.5 mmol/l |
| Urea | 2.5 – 7.5 mmol/l |
| Glucose | 3.5 – 5.0 mmol/l |
| Creatinine | 35 – 135 μmol/l |
| Alanine Aminotransferase (ALT) | 5 – 35 U/l |
| Gamma-glutamyl Transferase (GGT) | < 65 U/l |
| Alkaline Phosphatase (ALP) | 30 – 135 U/l |
| Aspartate Aminotransferase (AST) | < 40 U/l |
| Total Protein | 60 – 80 g/l |
| Albumin | 35 – 50 g/l |
| Globulin | 2.4 – 3.5 g/dl |
| Amylase | < 70 U/l |
| Total Bilirubin | 3 – 17 μmol/l |
| Calcium | 2.1 – 2.5 mmol/l |
| Chloride | 95 – 105 mmol/l |
| Phosphate | 0.8 – 1.4 mmol/l |
| Haematology | Normal Value |
|---|---|
| Haemoglobin | 11.5 – 16.6 g/dl |
| White Blood Cells | 4.0 – 11.0 x 109/l |
| Platelets | 150 – 450 x 109/l |
| MCV | 80 – 96 fl |
| MCHC | 32 – 36 g/dl |
| Neutrophils | 2.0 – 7.5 x 109/l |
| Lymphocytes | 1.5 – 4.0 x 109/l |
| Monocytes | 0.3 – 1.0 x 109/l |
| Eosinophils | 0.1 – 0.5 x 109/l |
| Basophils | < 0.2 x 109/l |
| Reticulocytes | < 2% |
| Haematocrit | 0.35 – 0.49 |
| Red Cell Distribution Width | 11 – 15% |
| Blood Gases | Normal Value |
|---|---|
| pH | 7.35 – 7.45 |
| pO2 | 11 – 14 kPa |
| pCO2 | 4.5 – 6.0 kPa |
| Base Excess | -2 – +2 mmol/l |
| Bicarbonate | 24 – 30 mmol/l |
| Lactate | < 2 mmol/l |
