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74
Manipal Manual of Surgery
• Visually check the blood bag for any obvious abnormalities, such as very dark blood or visible clots, and
if present, do not transfuse, and return it to the blood
bank. Check the date of collection and date of expiry
before transfusion. The storage shelf-life of red blood cells
depends on the preservative added (Key Box 18.2).
• Watch for any transfusion reactions.
Key Box 18.2
Storage of Blood
Preservative RBC survival
(days)
ACD (acid-citrate-dextrose) 21
CPD (citrate-phosphate-dextrose) 28
CPDA (citrate-phosphate-dextrose-adenine) 35
SAGM (saline-adenine-glucose-mannitol) 35
Whole blood transfusion is not advisable for routine
use and is also not available from blood banks. However,
there is some evidence in the literature that fresh whole
blood transfusion may be helpful in patients with
massive trauma, as all blood components are replaced
simultaneously to match the loss. However, this is
difficult practically, as the blood products still need to
be screened for various antigens and infections.
Other blood products available are fibrinogen
concentrate (high risk of hepatitis), factor VIII and
factor IX concentrates (for use in haemophilia and
Christmas disease, respectively) and factor VII
concentrate (for use in disseminated intravascular
coagulation—DIC).
COMPLICATIONS OF BLOOD TRANSFUSION
Treatment
• Stop the blood transfusion. Send the blood bag to the
blood bank and recheck.
• Repeat coagulation profile.
• IV fluids, monitor urine output, check urine for
.
Hb
• Diuresis with furosemide 20–40 mg IV or injection
mannitol 20% 100 ml IV to flush the kidney.
• If renal failure does occur, haemodialysis may be
required.
• If haemodynamically unstable, cardiovascular
support may be required.
Minor Incompatibility Reaction
• Occurs due to extravascular haemolysis.
• Usually mild, occurs at 2–21 days.
• Occurs due to antibodies to minor antigens.
• Malaise, jaundice, and fever.
• Treatment is supportive.
Nonhaemolytic Reactions
Febrile R
eaction
• Occurs due to sensitisation to WBCs or platelets
• Increased temperature—no haemolysis
• Use of 20–40 mm filter or leucocyte-depleted blood
may prevent it.
Allergic Reaction
• Occurs due to allergy to plasma products.
• Manifests as chills, rigors, and rashes all over.
• Often subsides with antihistamines, such as chlor-
pheniramine maleate 10 mg IV.
IMMUNE COMPLICATIONS
Haemolytic Reactions
Major (ABO) Incompatibility Reaction
• This is the result of mismatched blood transfusion.
• The majority of cases are due to technical errors, such
as sampling, labelling, dispatching.
• This causes intravascular haemolysis.
Clinical features
• Haematuria
• Pain in the loins (bilateral)
• Fever with chills and rigors
• Oliguria due to products of mismatched blood
transfusion blocking the renal tubules. It results in
Section I • Basic Principles of Surgery
acute renal tubular necrosis.
Transfusion-related Acute Lung Injury (TRALI)
It is a rare complication, that occurs within 6 hours of a
transfusion due to the presence of antileucocyte
antibodies in the transfused plasma, which cause the
patient’s white cells to aggregate in the pulmonary
circulation. This leads to degranulation of leucocytes,
causing increased capillary permeability and noncardiogenic pulmonary oedema. Symptoms may vary
from mild dyspnoea to full blown acute respiratory
distress syndrome. Proper supportive therapy will see
that it resolves within 24–48 hours.
Congestive Cardiac Failure (CCF)
CCF may occur, if whole blood is transfused rapidly,
especially in patients with chronic anaemia due to
circulatory overload.
Blood Transfusion
75
Treatment
• Slow transfusion, injection furosemide 20 mg IV.
• Packed cell transfusion is the choice in these
patients.
INFECTIOUS COMPLICATIONS
Serum hepatitis, AIDS, malaria, and syphilis are
dangerous infectious diseases that may be transmitted
from one patient to another through blood transfusion.
The danger is increased in cases of multiple transfusions
and in emergency situations. “Prevention is better than
cure”. Hence, it is mandatory to screen the blood for
these diseases before transfusion.
OTHER COMPLICATIONS
Citrate toxicity (causing hypocalcaemia), dilutional
coagulopathy (thrombocytopenia and dilution of clotting factors) can occur especially in massive tranfusion.
MASSIVE BLOOD TRANSFUSION
Definition: Massive blood transfusion has been defined
as follows:
• Replacement of >1 blood volume (or >10 units of
packed cells) in 24 hours.
• Half the patient’s blood volume in 6 hours.
• >4 RBC units in one hour with ongoing need for
transfusion, or
• 500 ml over 5 min with haemodynamic instability and
need for transfusion.
Massive blood loss may occur with trauma, post-
partum haemorrhage, or during major surgeries.
Massive transfusion protocol: In patients with massive
bleeding who are expected to require massive transfusion, the blood bank should be intimated to activate
massive transfusion protocol (MTP). A blood sample
must be sent for cross-matching with an initial request
for 2 units of red blood cells. After this, if MTP is
requested, the blood bank releases blood products in
different ‘boxes’ (Table 18.1).
The blood products are obtained box by box as
necessary. If the bleeding stops, the blood bank should
Table 18.1 Release of blood products on activation of MTP
Box PRBC FFP Platelet Cryoprecipitate
One 22 – –
Two 4 4 1 adult –
Three 44 – 3
Four 4 4 1 adult
be intimated immediately, so that MTP can be
terminated. If bleeding continues, boxes three and four
are alternately requested for. In such patients, regular
and half hourly measurements of acid–base status,
haemoglobin, platelets, prothrombin time (PT), activated partial thromboplastin time (aPTT), fibrinogen, and
serum calcium are required with an aim to normalise
their values. The use of thromboelastography or Rotem
allows visualisation of the process of clot formation and
helps identify specific defects. This is now being made
available as ‘point-of-care’ testing.
Disseminated Intravascular Coagulation (DIC)
• It occurs in massive blood transfusion, wherein all
factors of coagulation are consumed, resulting in a
bleeding disorder (consumption coagulopathy).
• It produces severe afibrinogenemia.
• It is treated by replacement with fibrinogen
(cryoprecipitate) and other clotting factors.
AUTOLOGOUS TRANSFUSION
This concept originated to avoid transfusion reactions that may develop when homologous blood is used.
• Here, the patient’s own blood is used.
Types of Autologous Transfusion
. Predeposit: 2–5 units of blood may be donated over
1
2–4 weeks before elective surgery.
2. Preoperative haemodilution: For cases like surgery
for thyrotoxicosis or abdominopelvic resection,
wherein one can expect 1–2 units of blood loss. Just
before surgery, 1–2 units of blood are removed, stored
in blood bags and serially numbered. Normovolaemia
is ensured by infusing 2–3 times the volume drawn
with crystalloids. The blood drawn is retransfused
in the reverse order after the procedure (the last bag
first and the first bag containing higher haematocrit
is given last).
3. Blood salvage: Blood which is lost during surgery is
collected, mixed with anticoagulant solution, washed,
and reinfused. This may be done, if the surgery does
not involve severe infection, bowel resection, or
malignancy, and does not contain materials such as
bone cement.
Advantage: All the risks involved with blood trans-
fusion are avoided.
Disadvantages
• May not be acceptable to the patient.
• Requires sophisticated equipment.
Section I • Basic Principles of Surgery
76
Manipal Manual of Surgery
Fig. 18.1: Blood products
Blood Products
Figure 18.1 depicts blood products.
Packed cells and fresh frozen plasma transfusion should not be
used to treat malnutrition.
Tranexamic acid is very useful as an antifibrinolytic agent to
reduce blood loss.
BLEEDING DISORDERS
Haemophilia
This is the most common bleeding disorder, which occurs
due to an X-linked genetic disorder of coagulation.
Types
1.
Haemophilia A: This results from a reduction of
factor VIII (anti-haemophilic factor) and is carried by
a recessive gene.
2. Haemophilia B: This results due to deficiency of
factor IX.
Haemophilia A
• ‘Excessive, unusual and unexpected bleeding’ during
surgery could be due to haemophilia ‘A’. This must
be confirmed with laboratory tests.
• A haemophilic patient’s daughters will be carriers,
but all sons will be normal.
• Thus, a carrier woman has 50% chance of producing
a haemophiliac male or a female carrier.
• The level of coagulation factor VIII in the blood may
be <1% of that in a normal individual.
Clinical Features
1. Bleeding into joints (haemarthrosis)
• Large joints, such as knees, elbows, ankles, and wrists
are affected.
• Spontaneous bleeding is common. It may also occur
due to minor trauma.
• Repeated bleeding may result in permanent damage
to the articular surfaces, resulting in deformity of the
Section I • Basic Principles of Surgery
joints.
Table 18.2 Blood changes in haemophilia A and von
Willebrand’s disease
Haemophilia ‘A’ von Willebrand’s
disease
Bleeding time Normal ↑
Prothrombin time Normal Normal
VIII: C ↓↓↓ ↓
vWF Normal ↓
2. Bleeding into muscles
• Calf muscle and psoas muscle haematomas are
common, resulting in contraction and fibrosis of
muscle, muscle pain, and weakness of the limb.
• Intramuscular injections should be avoided.
Investigations (Table 18.2)
Treatment
• Administration of factor VIII concentrate by intravenous
infusion is the treatment whenever there is bleeding.
• It should be given twice daily, since it has a half-life
of 12 hours.
• Any major surgical procedure should be carried out
only after raising factor VIII:C levels to 100% preoperatively, and it should be maintained >50% until
healing occurs.
• Synthetic vasopressin (DDAVP) produces a rise in
factor VIII:C.
Causes of Death
• Cerebral haemorrhage used to be the most common
cause of death in haemophiliacs. However, HIV infection seems to be the most common cause of death today.
• Hepatocellular carcinoma and cirrhosis due to HIV
and HCV also are the other causes (due to repeated
blood transfusions).
Haemophilia B (Christmas Disease)
• Incidence: One in 30,000 males. The inheritance and
clinical features are identical to haemophilia A.
• It is caused by a deficiency of factor IX.
• Treatment is with factor IX concentrates.
Blood Transfusion
77
von Willebrand’s Disease (vWD)
• In vWD, there is defective platelet function and factor
VIII:C deficiency due to a deficiency or abnormality
of vWF.
• Epistaxis, menorrhagia, and bleeding following
minor trauma or surgery are common.
• Haemarthrosis is rare.
• Treatment is similar to mild haemophilia. DDAVP,
IV infusion of factor VIII:C or vWF is required before
surgery.
A clinical haematologist must be consulted to help
optimise a patient with bleeding disorders for surgery.
HYPERBARIC OXYGEN
Hyperbaric oxygen is administered to patients when
their own haemoglobin is unable to carry adequate
oxygen or when hyperoxia is required. Hyperbaric O
is administered using either a monoplace (single patient)
or multiplace compression chamber.
Indications
1. Carbon monoxide poisoning: Hyperbaric O
2–3 atm is given to increase the O
dissolved in plasma
2
(5–6 ml/dl at 3 atm, whereas it is 0.3 ml/dl at
1 atm) which is sufficient to meet the O
requirement
2
of the body, even in the absence of normal haemoglobin (severe CO poisoning).
2. Infections such as gas gangrene: Hyperoxia suppresses
the growth of anaerobic organisms.
3. Cancer therapy to potentiate radiotherapy
4. Arterial insufficiency
5. Decompression sickness and air embolism: Hyperbaric oxygen reduces the size of air bubbles, and
rapidly eliminates nitrogen from the air bubbles.
Contraindications
Untreated pneumothorax: May expand with hyper-
2
baric O
, resulting in life-threatening tension pneumo-
2
thorax.
2
at
1. Which of the following statements about packed red
cells is true?
A. It has a haematocrit of 35%
. The volume in one adult bag is 500 mL
B
C. Shelf-life is 35 days with CPDA solution
D. It contains no plasma
2. Haemolytic reactions due to mismatched blood
transfusion include the following except:
A. Haematuria
. Pain in the loins
B
C. Fever with chills and rigors
D. Diuresis
3. Which of the following is decreased in disseminated
intravascular coagulation?
A. Prothrombin time
. Partial thromboplastin time
B
C. Bleeding time
D. Platelets
4. The following are true in haemophilia except:
A. Prothrombin time is unaffected
. Partial thromboplastin time is unaffected
B
C. Platelet count is unaffected
D. Bleeding time is unaffected
5. The following are true about blood products except:
A. Fresh-frozen plasma is given in severe liver
failure
. Cryoprecipitate is not used during massive
B
transfusion
C. Fibrinogen has a high risk of hepatitis
D. Factor VIII is used in haemophilia
6. The following are true about platelet transfusion
except:
A. They remain viable for 3–5 days
. Each unit will raise platelet count by 5–10,000
B
cells/mm
3
C. Platelets must be ABO compatible
D. Platelets may be low after heparin
Answers
1. C 2. D 3. D 4. C 5. B 6. C
Section I • Basic Principles of Surgery
19
Acid–Base Balance
Basic definitions
Henderson-Hasselbalch equation
Regulation of acid–base balance
SU9.1: Choose appropriate biochemical, microbiological,
pathological, imaging investigations and interpret the
investigative data in a surgical patient.
Please note: Here you can study the interpretation of ABG.
INTRODUCTION
Human blood has a hydrogen ion concentration [H+] of
35 to 45 nmol/L and it is essential that its concentration
is maintained within this narrow range. Hydrogen ions
are nothing but protons which can bind to proteins and
alter their characteristics. All the enzymes present in
the body are proteins and an alteration in these enzyme
systems can change the homeostatic mechanisms of the
body. Hence, a disturbance in acid–base balance can
result in malfunction of the various organ systems.
BASIC DEFINITIONS
What is pH?
pH notation is a more common method of expressing
the hydrogen ion concentration. It is defined as the
negative
mol/L. pH of blood = 7.4.
What is an acid? What is a base? What is a buffer?
• An acid is
• A base
• A buffer
logarithm to base 10 of the [H
a substance that dissociates in water to
+
produce H
conjugate base. By combining with a strong acid or a
.
is a substance that accepts H+.
is a combination of a weak acid and its
+
] expressed in
Acid–base disorders
Rapid interpretation of an ABG report
strong base, they produce the corresponding salt and
a weak acid or a weak base, respectively.
For example: A weak acid, such as carbonic acid with
its conjugate base, sodium bicarbonate, is called the
bicarbonate/carbonic acid buffer system. When a
strong acid, such as hydrochloric acid, is added to
the solution, it combines with the weak alkali (sodium
bicarbonate) to form sodium chloride and carbonic
acid. When a strong base, such as sodium hydroxide
is added, it combines with the weak acid (carbonic
acid) to form sodium carbonate and water. Thus, a
strong acid and a strong base are converted into a
weak acid and a weak base by the bicarbonate/
carbonic acid buffer system.
The hydrogen ion concentration of blood is
maintained within narrow limits because of the presence
of buffers in the body. These natural buffers are of two
types: Extracellular and intracellular.
• The extracellular buffers are bicarbonate/carbonic
acid buffer system, phosphate buffer system and
plasma proteins. The intracellular buffers are
haemoglobin and other proteins.
• The most important buffer system in the body is the
bicarbonate–carbonic acid buffer system. This is
because of the ability of the body to maintain or alter
the concentrations of its two components separately.
The concentration of carbonic acid is regulated by
respiration wherein the excess carbonic acid is
eliminated
bicarbonate concentration is independently regulated
by the kidneys.
as carbon dioxide by the lungs. The
78
Acid–Base Balance
–
79
THE HENDERSON AND HENDERSON-
HASSELBALCH EQUATIONS
The hydrogen ion concentration is proportional to the
concentration of buffer systems of the body. The
hydrogen ion concentration, carbonic acid levels and
the bicarbonate levels of blood are related according to
the following equation:
HCO(mmol/L)
+
] (nmol/L) =
[H
23
K×
–
HCO (mmol/L)
3
where K = constant. This equation is called the
Henderson equation.
The amount of carbonic acid in the blood is directly
proportional to the partial pressure of carbon dioxide
in the blood. Thus, the carbonic acid concentration is a
product of the partial pressure of carbon dioxide in
blood and its solubility coefficient.
[H
carbon dioxide in blood and PCO
] = α PCO2, where α = solubility coefficient of
2CO3
is the partial pressure
2
of carbon dioxide in blood.
α = 0.03 ml/mmHg/100 ml blood and normal PCO
= 40 mmHg
[H
] = α PCO2 = 0.03 × 40 = 1.2 ml/dl.
2CO3
K = 800 for the carbonic acid/bicarbonate buffer
system. The normal bicarbonate level of blood is
24 mmol/L.
+
] (nmol/L) =
[H
800 ×1.2
24
=40nmol/L
The Henderson equation can also be written as
follows.
α
PCO (mmHg)
+
] (nmol/L) =
[H
K
×
2
HCO
–
3
From this equation, it is evident that the hydrogen
ion concentration increases when the PCO2 increases
–
or when the [HCO
] levels decrease. Similarly, a
3
decrease in hydrogen ion concentration occurs when
the PCO
decreases or when the [HCO
2
–
] levels increase.
3
When expressed in logarithmic form, the Henderson
equation is written as follows:
–
[HCO ]
pH =
pK log
+
a
3
[H CO ]
23
This logarithmic version of Henderson equation is
called the Henderson-Hasselbalch equation.
The pK
(negative logarithm of the constant K) of the
a
carbonic acid/bicarbonate buffer system is 6.1.
pH = 6.1 + log 24/1.2
= 6.1 + log 20 = 6.1 + 1.3 = 7.4
+
It is important to appreciate that the [H
+
inversely related. When the [H
] rises, the pH decreases
] and pH are
and vice versa.
REGULATION OF ACID–BASE BALANCE
The normal pH of blood is 7.35–7.45. Acidosis is defined
as a pH less than 7.35. Conversely, when the pH is more
than 7.45, alkalosis is said to exist. Acidosis and alkalosis
are of two types each—respiratory and metabolic.
An increase in carbon dioxide (CO
the plasma [H
+
] and decreases the pH (respiratory
) levels increases
2
acidosis). Similarly, a decrease in plasma carbon dioxide
+
levels reduces the [H
alkalosis). A decrease in [HCO
] and increases the pH (respiratory
–
] reduces the pH and is
3
called metabolic acidosis. Similarly, an increase in
–
[HCO
] increases the pH and produces metabolic
3
alkalosis.
The pH is regulated in the human body mainly by
two organs: The respiratory system and the renal system.
The arterial carbon dioxide levels are regulated by
the respiratory system. Any increase in carbon dioxide
levels stimulates the respiratory centre in the medulla
thus augmenting respiration, alveolar ventilation and
elimination of extra CO2 levels. A decrease in CO2 levels
2
may reduce the stimulus to breathe and cause hypoventilation. This response is limited by hypoxia as the
hypoxic drive stimulates the patient to maintain
respiration. Respiratory response to changes in CO2 level
occurs very fast.
The plasma bicarbonate levels are regulated by the
kidneys. Any decrease in [HCO
–
] stimulates the
3
kidneys to retain and synthesise bicarbonate. High
–
[HCO
] results in elimination of more bicarbonate in
3
urine. In general, the pulmonary response to a change
in acid–base status is faster and occurs immediately.
However, renal regulation takes time, a few hours to
days. Kidneys filter and reabsorb all the bicarbonate
in the urine. When necessary, kidneys can also
produce extra bicarbonate through the glutamine
pathway.
ACID–BASE DISORDERS
When an acid–base disorder occurs, the initial disturbance that occurs is termed the primary disorder.
The body attempts to normalise the pH by certain
compensatory mechanisms resulting in a secondary
disorder, e.g. primary metabolic acidosis results in an
increase in hydrogen ions and a consequent decrease
in bicarbonate ions. To compensate for this, the patient
hyperventilates and reduces the arterial carbon dioxide
levels, thus moving the pH back to normal (compensatory respiratory alkalosis).
Thus, there are four primary disorders and four
secondary disorders (Key Box 19.1).
Section I • Basic Principles of Surgery
80
Manipal Manual of Surgery
Key Box 19.1
Primary Disorder Secondary Disorder
Respiratory acidosis Metabolic alkalosis
Respiratory alkalosis Metabolic acidosis
Metabolic acidosis Respiratory alkalosis
Metabolic alkalosis Respiratory acidosis
RESPIRATORY ACIDOSIS
Causes
This disorder occurs when the patient’s ability to
maintain minute ventilation is compromised. This may
be acute or chronic in origin. The causes may be
classified as follows:
• Central nervous system: Central nervous system
depression due to trauma, tumour, infections,
ischaemia or drug overdose. Spinal cord injuries,
especially cervical or high thoracic, can cause
respiratory muscle paralysis.
• Peripheral nervous and muscular systems: Guillain-
Barré syndrome, tetanus, organophosphorus
poisoning, poliomyelitis, myasthenia gravis.
• Primary pulmonary disease: Asthma, chronic obstruc-
pulmonary disease, acute respiratory distress
tive
syndrome, pneumonia.
• Loss of chest wall integrity: Flail chest.
Key Box 19.2
Hyperventilation
Head injury
Hydrogen ions (metabolic acidosis)
Hyperpyrexia
Hysteria
High altitudes
Causes (Key Box 19.2)
• Supratentorial lesions: Head injury
• Fever
• Pain
• Anxiety, hysterical hyperventilation
• High altitudes
• It may also occur secondarily as a compensation to
primary metabolic acidosis.
Features
• Usually features of the underlying disease predomi-
nate the picture.
• Acute severe hypocarbia (PaCO
<20 mmHg) may
2
cause cerebral vasoconstriction, reduced cerebral
blood flow, confusion, seizures and tetany.
• The alkalosis and consequent hypokalaemia can also
cause cardiac arrhythmias.
Clinical Features
• The features of the underlying problem predominate
the clinical picture.
• If acute, hypoxia and hypercarbia result in tachycardia,
hypertension, arrhythmias, confusion, drowsiness
and coma. The hypoxia, if untreated, can be fatal.
• If gradual in onset, as in chronic obstructive pulmo-
nary disease (COPD), the patient’s kidneys may
compensate by retaining bicarbonate resulting in
compensatory metabolic alkalosis. Arterial blood gas
analysis in these patients typically shows low PaO
high PaCO
, high bicarbonate levels and a near-
2
normal pH.
Treatment
• Treat the cause.
• Maintenance of oxygenation and ventilation using
mechanical ventilatory support till recovery of the
primary problem occurs.
RESPIRATORY ALKALOSIS
This occurs due to an increase in minute ventilation.
This increase can be sustained only in abnormal
conditions. This may be acute or chronic in origin.
Section I • Basic Principles of Surgery
METABOLIC ACIDOSIS
Causes
This is associated with a decrease in bicarbonate ions
due to one of two reasons:
. Overproduction or retention of non-volatile acids
1
in the body, as in:
• Diabetic ketoacidosis
• Lactic acidosis
• Salicylate poisoning, methanol poisoning
• Renal failure
,
2
. Loss of bicarbonate ions from the body as in
2
• Diarrhoea
• Intestinal fistulae
Features
• Usually features of the underlying disease predomi-
nate the picture.
• Hypotension, reduced cardiac output
• Hyperventilation—rapid, deep respirations
• Deep, gasping type of respiration seen in diabetic
ketoacidosis is called
Kussmaul’s respiration.
• Hyperkalaemia, arrhythmias
• Lethargy, coma
Acid–Base Balance
Metabolic acidosis can be of high anion gap or normal
anion gap type.
Anion Gap
The law of electroneutrality states that the total number
positive charges must be equal to the total number
of
of negative charges in the body fluids. Thus, cations
(positively charged ions such as sodium and potassium)
must produce a charge exactly balanced by anions.
However, the concentrations of only sodium, potassium,
chloride and bicarbonate ions are routinely measured
in clinical practice. The number of the measured cations
+
) exceeds the sum of measured anions (Cl– and
(Na
–
HCO
) producing a ‘deficit’ called the ‘anion gap’
3
(Fig. 19.1). The normal anion gap is 9–14 mmol/l. This
gap is due to the presence of unmeasured anions in the
body.
Fig. 19.1: Normal anion gap. The main cation is sodium (shown
as blue circles) and the main anions are chloride ions (yellow
circles) and bicarbonate (red circles).
Since the extracellular concentrations of potassium is
small, it is often ignored in the calculation of anion gap.
Anion gap may be used to distinguish the cause of
metabolic acidosis.
Causes of high anion gap acidosis: MUDPILES
(methanol, uraemia,
diabetic ketoacidosis, paracetamol/
propylene glycol, iron/isoniazid, lactic acidosis,
ethylene glycol, salicylate poisoning).
• Anion gap is increased (>14
mmol/L) in metabolic
acidosis due to an increase in fixed acid load. These
acids react with the bicarbonate ions in the plasma
lowering its concentration. This results in high anion
gap metabolic acidosis (HAGMA) (Fig. 19.2).
81
Fig. 19.3: Normal anion gap metabolic acidosis. Note the loss
of bicarbonate ions (red circles) and their replacement with
chloride (yellow circles)
• Anion gap remains unchanged in metabolic acidosis
due to loss of bicarbonate ions as the lost bicarbonate
ions are replaced by chloride ions. There is no change
in the measured anion concentration and thus, the anion
gap remains normal (Fig. 19.3). This type of metabolic
acidosis is also called ‘hyperchloraemic metabolic
acidosis’. Example: Diarrhoea, renal tubular
acidosis.
• Corrected anion gap: The anion gap (AG) can be
falsely low in hypoalbuminaemia, a common clinical
condition in the critically ill. Adjust anion gap for
albumin as given below:
Adjusted AG = Observed AG + 2.5 × [4.5 – measured
albumin (g/dl)]
Treatment
• Identify the cause and treat.
• Ensure adequate ventilation.
• If pH <7.1 and the patient is unstable, may administer
sodium bicarbonate. The chances of life-threatening
arrhythmias are reduced when pH is >7.2.
Bicarbonate required (mmol/L) =
15 – measured [HCO
(Each ml of 8.4% NaHCO
of HCO
0.9 mmol of HCO
. Each ml of 7.5% NaHCO3 solution contains
3
–
).
3
–
] × 0.6 × Body wt (kg)
3
solution contains 1 mmol
3
Half the calculated dose of bicarbonate should be
given slowly and should be followed up with repeat
blood pH measurements as required.
METABOLIC ALKALOSIS
Fig. 19.2: Illustration of high anion gap acidosis. Note the loss of
bicarbonate ions (red circles)
Causes of normal anion gap acidosis: Diarrhoea,
isotonic saline infusion, early renal failure, renal tubular
acidosis, ureteroenterostomy.
Causes
This may be either due to loss of acid from the body or
retention of bicarbonate. It may be due to:
• Loss of gastric hydrochloric acid as in vomiting,
prolonged nasogastric drainage.
• Retention of bicarbonate in exchange for loss of
chloride ions as in diarrhoea.
• Excessive loss of H
+
from kidneys in exchange for K
in severe hypokalaemia.
• Primary or secondary hyperaldosteronism.
• Excessive exogenous administration of alkali, e.g.
indiscriminate use of NaHCO
, antacid abuse.
3
+
Section I • Basic Principles of Surgery
82
Manipal Manual of Surgery
Features
It is one of the common acid–base disorders in the
intensive care unit. The underlying problem gives a
clue
to the cause of metabolic alkalosis. When severe, it can
cause hypoventilation and seizures. Associated hypokalaemia can cause arrhythmias and contribute to
difficulty in weaning patients off a ventilator.
Treatment
• Treat the primary problem.
• Most of the metabolic alkaloses are ‘chloride-
responsive’.
Administration of saline and correction
of potassium deficits reduce the alkalosis.
• Chloride deficit (mmol)
–
= 0.2 × Body weight (kg) × (100 – serum Cl
)
• The calculated deficit can be replaced over 24 hours
using 0.9% saline (contains 154 mmol/L of chloride)
• Chloride unresponsive alkalosis may be due to hypo-
kalaemia or hypomagnesemia. Treat them.
COMBINED DISORDERS
In some clinical situations, patients can have combined
disorders. HAGMA and NAGMA can co-exist (Fig. 19.4).
Similarly, metabolic acidosis and alkalosis can be
present in the patient at the same time (Fig. 19.5). Hence,
whenever a patient presents with HAGMA, check
whether there is a co-existing disorder.
A ‘gap-gap analysis’ helps in identifying whether
HAGMA is associated with other disorders.
Gap-Gap
= (12 – measured anion gap)/24 – measured HCO
–
3
If the ratio is 1, infer that the patient has HAGMA.
If <1, there is co-existing NAGMA with HAGMA.
If >1, there is co-existing HAGMA and metabolic
alkalosis.
RAPID INTERPRETATION OF AN ABG REPORT
Analysis and conclusion of arterial blood gas (ABG)
report must always be done in conjunction with history
and clinical examination. ABG analysis is done to assess:
. Oxygenation status
1
2. Ventilatory status
3. Acid–base status
Oxygenation
The partial pressure of oxygen in arterial blood (PaO2) of
a normal, healthy, young adult is usually 90–100 mmHg.
While assessing oxygenation, the PaO
related to ispired oxygen concentration (FIO
must always be
2
).
2
An easy bedside assessment of oxygenation can be
made using a PaO2/FIO2 ratio (Key Box 19.3). The ratio
can also be used to evaluate the response to therapy.
Key Box 19.3
PaO2/FIO2 ratio Status of oxygenation
≥500 Normal
250–500 Adequate
100–250 Poor
<100 Critical
A pulse oximeter is helpful to assess whether the
patient’s oxygenation is life-threatening or not. A
)
saturation of 98–100% may be reassuring. However,
early changes in the oxygenation status may be missed,
if one relies on a pulse oximetry and the patient is
breathing high concentrations of oxygen. This is because
of the sigmoid
where the SaO
shape of the oxygen dissociation curve
will be 99–100%, whether the PaO2 is
2
100 mmHg or 500 mmHg. Hence, an arterial blood
gas analysis must
always be obtained whenever a
doubt exists about the oxygenation status of the patient.
Fig. 19.4: A combination of HAGMA and NAGMA. Bicarbonate
ions are lost producing HAGMA but some of them are replaced
by chloride ions (NAGMA).
Fig. 19.5: In this case, bicarbonate ions are lost producing HAGMA
but the patient has lost chloride ions as well (excessive vomiting).
Section I • Basic Principles of Surgery
Ventilation
The normal PaCO
is 35–45 mmHg. The PaCO2 must
2
always be related to the alveolar ventilation of the
patient. The minute volume of a normal healthy adult
at rest would be 100 ml/kg/min. Sixty to sixty-five per
cent of this actually ventilates the alveoli, the rest is dead
space ventilation.
If the alveolar ventilation decreases (either due to a
decrease in minute volume or an increase in dead space
ventilation), the arterial PaCO
hand, the arterial PaCO
2
will rise. On the other
2
may remain normal but the
patient’s minute volume may have increased.
Acid–Base Balance
83
Do not assume that the patient must be well when
the PaCO
is normal. A clinical examination of the patient
2
is necessary to rule out respiratory distress (dyspnoea,
tachypnoea, active accessory muscles of respiration,
tracheal tug, flaring of alae nasi, etc.). The patient may
not be able to sustain this increased levels of ventilation
for a prolonged period of time, is likely to get exhausted
and may require mechanical ventilatory support.
Acid–Base Status
The assessment of acid–base status must be done in
three steps and in the following order.
a. Assess the pH first: Normal pH—7.35 to 7.45. If the
pH is less than 7.35, the patient has acidosis and if it
is more than 7.45, the patient is alkalotic. The direction
of change in pH shows the primary disorder. This is
because the compensatory mechanisms never overshoot the requirement of reaching the normal pH.
b. Assess the PaCO
normal PaCO
but the PaCO
next: Is the PaCO2 normal? The
2
is 35–45 mmHg. If the pH is abnormal
2
normal, it suggests a metabolic dis-
2
order. However, the body usually tries to compensate
for a change in pH. The respiratory compensation is
early and fast.
If the changes in pH and PaCO
are in opposite direc-
2
tions (one is increased and the other decreased), the
primary disorder is respiratory. If the changes in pH
and PaCO
are in the same direction (both are increased
2
or decreased), the primary disorder is metabolic.
For example, if the pH is 7.2 and the PaCO
2
is
60 mmHg, the decrease in pH suggests acidosis. The
PaCO
has moved in the opposite direction (increased)
2
and suggests respiratory acidosis. Similarly, if the pH
is alkalotic and the PaCO
is low, it suggests primary
2
respiratory alkalosis.
A change in PaCO2 also changes the serum bicarbo-
nate concentration (Key Box 19.4).
Key Box 19.4
Condition PCO
Acute respiratory acidosis 10 mmHg↑↑1 mmol/L
Acute respiratory alkalosis 10 mmHg↓↓2 mmol/L
Chronic respiratory alkalosis 10 mmHg↓↓5 mmol/L
2
[HCO
–
]
3
and acidosis
Key Box 19.5
Metabolic acidosis: Expected ΔPaCO2 = 1.2 × Δ[HCO
Metabolic alkalosis: Expected ΔPaCO2 = 0.7 × Δ[HCO
–
]
3
–
]
3
Metabolic disorders: Changes in serum bicarbonate
concentration is accompanied by compensatory changes
in PaCO
(Key Box 19.5).
2
As described previously, whenever metabolic
acidosis is present, calculate anion gap to help diagnose
the type of metabolic acidosis (high anion gap or normal
anion gap). Similarly, when a patient has metabolic
alkalosis, assess whether it is chloride responsive or
unresponsive type and treat accordingly.
It must be remembered that these are general
guidelines applicable to patients who are breathing
spontaneously. These are useful for rapid bedside
assessment of acid–base status. Occasionally, the
patients can present with different combinations of
acid–base disorders such as a mixed respiratory and
metabolic alkalosis, or a mixed respiratory and metabolic acidosis.
In critically ill patients with multiorgan failure such
as renal and respiratory abnormalities and receiving
mechanical ventilation, the physiology can be very
complicated. Mixed disorders are common in such
patients and a more detailed analysis as described
previously may be required.
1. A 30-year-old man was admitted to the ICU with history
of consumption of organophosphorus poisoning 4 hours
ago. On admission, he is drowsy, breathing 60%
oxygen by face mask and has a bradycardia. A blood
gas analysis taken half an hour later shows a PaO
= 100 mmHg, PaCO2 = 60 mmHg and a pH of 7.24.
Analysis
Oxygenation: The PaO2 on 60% oxygen should have
been about 300 mmHg. The PaO2/FIO2 ratio in this
patient is 100/0.6 = 167. Thus, although the PaO2 is
adequate to sustain life, the patient’s oxygenation
status is poor.
Ventilation: Raised PaCO2 suggests respiratory
acidosis.
Acid–base status: The pH shows acidosis. The pH has
decreased, whereas the PaCO2 has increased. Hence, the
patient has primary, uncompensated respiratory acidosis.
2. A 60-year-old man, a known diabetic since the last
2
15 years is admitted with diabetic ketoacidosis. He
required endotracheal intubation and ventilation with
60% oxygen. An arterial blood gas analysis shows the
following:
PaO2 = 60 mmHg, PaCO2 = 28 mmHg, pH = 7.14 and
–
[HCO
] = 12 mmol/l
3
Analysis
Oxygenation: The PaO2 on 60% oxygen should have
been about 300 mmHg. The PaO2/FIO2 ratio in this
patient is 60/0.6 = 100. Thus, although the PaO2 is just
adequate to sustain life, the patient’s oxygenation is poor.
Section I • Basic Principles of Surgery