Surgery Vol 1 2021 Cairo University @AUDatabot.pdf
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Chapter 2: Major Trauma and the Multiple-Injury Patient - Introt Unnessary IVE CHAPTER 2 MAJOR TRAUMA AND THE MULTIPLE-INJURY Bulloint management PATIENT ER management Introduction: CHAPTER CONTENTS Trauma is a common cause of mortality both in civilian life and during war time. It is the lead...
Chapter 2: Major Trauma and the Multiple-Injury Patient - Introt Unnessary IVE CHAPTER 2 MAJOR TRAUMA AND THE MULTIPLE-INJURY Bulloint management PATIENT ER management Introduction: CHAPTER CONTENTS Trauma is a common cause of mortality both in civilian life and during war time. It is the leading cause of death for individuals of age 1-44 years, and ranks third in causing mortality in all ages. In addition, it is a major cause of morbidity. For every trauma death, two people suffer permanent disabilities. Major trauma commonly causes multiple injuries in different parts of the body. • • • • • • • Introduction Mechanism of injury Causes of trauma mortality Organized trauma care Primary survey/resuscitation Secondary survey Definitive treatment of individual injuries Mechanism of injury: There are two major types of injuries: 1. Penetrating injuries: • Low velocity injuries. These are caused by: o Knives, spikes of glass, and other sharp objects. o Bullets that are fired by pistols travel at a slow velocity and are, therefore, included in this group. The injury is usually focused over a small area. • High velocity injuries. The common example is firearm injuries that are caused by rifles. Here the energy may be dissipated over a wide area. Shock waves spread out from the main missile tract and affect areas far from the primary missile tract. The higher the velocity of the missile, the more is the damage it causes (chapter 1). • • • • Trauma care principles There is a need for rapid evaluation of the trauma patient. Time wasted costs lives. The absencP. of a definitive diagnosis should never impede the application of lifesaving measures. Management in the first 'Golden Hour' is crucial to both the short and long term survival of the patient. It is also critical in determining the morbidity that the patient will endure. There is a need to establish management priorities. The things which will kill the patient first are always the things which should be checked and treated first. Things which will kill the patient later are managed later. Thus, airway problems are managed and treated before breathing problems, which in turn are treated before circulatory problems. 2. Blunt injuries: • Direct blows • Fall from a height • Road traffic accidents (RTA) When a pedestrian is struck by a moving vehicle, there is often an acceleration injury in addition to the direct trauma at the site of impact. A person inside a moving car acquires the same velocity of the car. If the car stops suddenly, the person will continue moving forwards and if he is not wearing the seat belt, the head will strike against the car. The force Fig. 2_1_The seat beit mark.Suspect of impact of the body against the seat belt may seat belt in·uries itself cause fracture of the clavide, damage to .___ _ _ _..;...c.___,____ _ __ , - Chapter 2: Major Trauma and the Multiple-Injury Patient the small intestine, the mesentery, stomach or duodenum, the so-called seat belt injuries. The skin mark of the seat belt should raise suspicion of such injuries (Fig. 2.1 ). It should be noted, however, that the protective benefits of a seat belt far exceed its possible injurious effect. With blunt trauma there is a tendency for certain patterns of associated injuries, e.g., a combination of head and cervical injuries, sternal and dorsal spine injuries, fracture of the lower ribs and rupture of the liver or spleen, and pelvic fracture with bladder or urethral injuries. Causes of trauma mortality: Deaths following trauma can be classified into 3 groups according to the timing after the accident. Immediate deaths: These follow fatal injuries and occur within few minutes after the accident so that lift le can be done for the victims. Examples & these injuries include major trauma to the brain or upper spinal cord, injuries of the heart or major blood vessels or rupture of the major airway. Early deaths: These occur within few hours after the accident and so, with proper and rapid management, the patients have a chance of survival. These cases include intracraniai haemorrhage, massive intra-abdominal or intrathoracic haemorrhage, or major fractures. Late deaths: These occur some weeks after the injury, generally due to sepsis or multiple organ failure. Organized systems for trauma care are focused on saving a trauma victim from early mortality, while critical care is designed to prevent late trauma mortality. Organized trauma care: Victims of major trauma are best treated by a well-organized and trained trauma team. Accident and emergency departments should have an equipped resuscitation area set aside to receive major trauma victims. In mass casualty accidents, e.g., train accidents or earthquakes, the concept of triage is important. Triage means sorting of patients, i.e., their ranking according to both their clinical need and the available resources to provide treatment. It may take two forms: o If the number of casualties does not exceed the facilities all critically ATLS 1. Primary survey/resuscitation. injured are treated. o If the number of casualties exceeds 2. Secondary survey. 3. Definitive treatment. facilities, then the critically injured Ainvay obstruction may kill the trauma most likely to survive are treated victim within minutes. Its relief should first. receive top priority. The American College of Surgeons developed the Advanced Trauma Life Support (ATLS) which is an internationally accepted protocol for the management of major trauma victims. ATLS protocol has three elements o Primary survey resuscitation. o Secondary survey. o Definitive treatment of individual injuries. This will be discussed in the corresponding chapters. Chapter 2: Major Trauma and the Multiple-Injury Patient - • The primary survey and resuscitation should start at the site of accident by trained ambulance personnel. It continues as the trauma victim reaches the hospital. Primary survey/resuscitation: Objective: The objective is to identify and treat any immediately life-threatening condition. Steps In sequence the five steps of the primary survey are A, B, C, D, E. A. Airway (and cervical spine control). B. Breathing. C. Circulation with haemorrhage control. D. Disability (brief neurological assessment). E. Exposure and Environment. Life-threatening problems discovered during the primary survey are always dealt with before proceeding to the secondary survey. A. Airway (and cervical spine control): The patient's airway is evaluated and protected if necessary, while concomitantly controlling movement of the cervical spine. In general, if the patient is capable of unstrained speech, his airway is patent. All patients receive supplemental oxygen by mask upon arrival. Clear the airway: 1. Vomit, blood or foreign material should be removed manually (finger sweep) or with a rigid sucker. 2. This is followed by chin lift or jaw thrust (Fig. 2.2). Protect the airway: Fig. 2.2. Clear the airway: Finger sweep • An oropharyngeal or nasopharyngeal airway tube Chin lift prevents the tongue from falling back and occluding the • Jaw thrust airway in an unconscious person. • Tracheal intubation is indicated with • Apnoea • Risk of aspiration • Impending or actual airway compromise (inhalation injuries, maxillofacial trauma) • Closed head injuries (allow hyperventilation to decrease intracranial pressure [ICP]) • Orotracheal intubation allows the use of a .. large tube. • Nasotracheal intubation is safer if the cervical spine appears fractured. • Cricothyroidotomy (Fig. 2.3). This is done either by making a cut and insrting a tube, or by the percutaneous insertion of a wide-bore needle. This procedure is not suitable for children. Fig. 2.3. Cricothyroidotomy N.B. Tracheostomy is rarely needed in the emergency room management. 111111119 Chapter 2: Major Trauma and the Multiple-Injury Patient Cervical spine control: The cervical spine should be considered unstable (pending radiological diagnosis) in the following situations: • Clinical examination reveals bony abnormalities or cervical tenderness. • Multisystem trauma, a blunt injury above the clavicle, or an altered level of consciousness from trauma or from drug/alcohol intake. • Maxillofacial trauma. Cervical spine immobilization is done using a backboard and a rigid collar. If a collar is not available, manual in-line immobilization is necessary (Fig. 2.4 ). Radiological evaluation is done later after stabilization of vital systems. At least three views of the cervical spine (lateral, AP, and odontoid) are done. Adl"I..I•• u,pe •c,oce foralloed 10 lrol!Oy Fig. 2 4. Cervical spine immobilization B. Breathing: Assessment: 1. Inspection for air movement, respiratory rate, cyanosis, tracheal shift, jugular venous distention, open chest wounds, asymmetric chest expansion and use of accessory muscles of respiration. 2. Palpation for subcutaneous emphysema and flail segments. 3. Auscultation for upper airway sounds (stridor, wheezing, or gurgling) and for lower airway sounds present over lung fields. 4. Percussion for hyperresonance or dullness over either lung field. The immediately life 4 hreatening thoracic conditions and their treatment are: 1. Tension pneumothorax. Needle decompression followed later by intercostal chest tube (Fig. 2.5). 2. Cardiac tamponade. Needle pericardiocentesis (Fig. 2.6) followed later by operative pericardiotomy and control of source of bleeding. Fig. 2.5. An intercostal chest tube is 3. Flail chest caused by fractures of adjacent ribs. This is used to drain air or fluid from the commonly associated with lung contusion. Emergency pleural cavity. The tube is connected to an under-water seal treatment includes stabilization of the flail segment by cotton guaze and adhesive bandage. 4. Massive haemothorax. Initial treatment is by chest tube insertion to allow lung expansion. Later thoracotomy may be needed if bleeding continues. 5. Open pneumothorax. Initial treatment is by an occlusive dressing fixed at 3 sides only followed by insertion of a chest tube. C. Circulation: Shock 1. Haemorrhagic. Commonest. Tension pneumothorax reduces venous return and worsens this shock. 2. Cardiogenic. Tamponade and myocardial trauma. 3. Neurogenic. Spinal cord injury. Chapter 2: Major Trauma and the Multiple-Injury Patient - Action 1. Bleeding is controlled with direct pressure if possible. Sites of hidden haemorrhage are intraabdominal, intra-thoracic, and fractures of pelvis and femur. 2. Two large-calibre (16 gauge) peripheral IV lines are inserted. A central line may also be added. 3. Blood samples are sent for typing, cross-matching, haemoglobin, haematocrit and blood chemistry. 4. Ringer's lactate solution is infused as a start. Volume of crystalloid needed = 3 X estimated blood loss. 5. When cross-matched blood is available it is to be infused immediately. IV fluids and blood are given at a rate that ensures an optimum urine output of 0.5-1 ml/kg/hour for adults. Fig 2.6. Pericardiocentesis for aspiration of blood from the pencardium. The needle is inserted to the left of xiphoid and is di reeled to the ti of left sea ula. D. Disability: (brief neurological assessment) Common causes of neurological deficits related to trauma are: • Head injury. • Hypoxia. • Shock. • Alcohol or drugs abuse. AVPU evaluation: Based on patient's best response. A. Alert and interactive V. Vocal stimuli elicit a response P. Painful stimuli are necessary to evoke a response U. Unresponsive This provides only brief neurological information. A more detailed assessment using the Glasgow Coma Scale (GCS) is performed during the secondary survey. E. Exposure and environment: Clothes: All clothes of the trauma victim are removed using sharp large scissors. Warmth: Keeping the emergency room warm and using blankets to prevent hypothermia, Insert • Urethral catheter (Foley's) to monitor urine output. This is contraindicated if there is blood at the urethral meatus as it indicates urethral injury. Trial of a catheter insertion in this case is usually unsuccessful and may even compound the injury. • Nasogastric tube (Ryle's) decompresses the stomach and prevents vomiting and aspiration. Radiological assessment: • For blunt trauma cervical spine (Fig. 2.7), AP chest Fig. 2.7. Cervical spine Xray shows fracture dislocation between CS and C6. Fig. 2.8. Chest X-ray of a major trauma victim shows a widened mediastinum which denotes aortic ru lure Chapter 2: Major Trauma and the Multiple-Injury Patient (Fig. 2.8) and AP pelvis (Fig. 2.9) X-rays are mandatory. For penetrating trauma, AP chest and X-ray of trauma site, if applicable. After resuscitation other X-rays or CT scans are performed as indicated. History: The patient's history should be obtained while completing the primary survey. If the patient is unconscious, the rescue team, accident witnesses, and family members should be relied upon to get the following information that have the acronym AMPLE. A. Allergies M. Medications P. Past medical history L. Last meal (time) E. Events of injury. Fig. 2.9. X-ray of the pelvis shows an unstable fracture of the pelvis, which is likely to be accompanied by bladder or osterior urethral in·ur Secondary survey: The secondary survey is to be done once resuscitation efforts are nder way and preliminary X-rays have been evaluated. Objectives: 1. Examination of the patient from head to toe and front to back. 2. Taking a complete medical history. 3. Integration of all clinical, laboratory, and radiological information. 4. Formulation of a management plan. It includes examination of: 1. Head. Haematoma, fractures and pupils. 2. Face 3. Spine. To allow examination of the back the patient's body is turned in one piece (log rolling) by four persons. This is to avoid injury of the spinal cord if there is an unstable spine fracture. 4. Neck 5. Chest 6. Abdomen: For indications of abdominal Fig. 2.10. CT scan of abdomen shows a tear in the spleen. The lower picture shows the exploration see chapter 40. CT (Fig 2.10) s lenic in·ur at abdominal ex !oration. or Diagnostic peritoneal lavage (DPL) are indicated in blunt abdominal trauma, in an adult, that is associated with: Suspicion of organ injury with equivocal signs. Unreliable abdominal examination because patient is unconscious, e.g., head trauma, or drug or alcohol intoxication. Unexplained hypotension that may be caused by blood loss. The technique, interpretation and limitations of DPL are discussed in chapter 40. Chapter 2: Major Trauma and the Multiple-Injury Patient 161111 7. Perineum, including rectal examination in all patients and vaginal examination in females. 8. Limbs for fractures and for soft tissuo injuries including vessels, nerves, and tendons, 9. Nervous system a. Pupils for size, equality, and reaction to light. b. Glasgow Coma Scale (see chapter 19). c. Cranial nerves. d. Sensation and motor activity in limbs. e. CT scan of head if there is suspicion of intra-cranial injuries (Fig. 2.11 ). Definitive treatment of individual injuries: This will depend upon the type of injury and willbe discussed in the relevant chapters. During this phase the following should be noted: Fig. 2.11. CT scan of head shows an extradural haematoma 1. Some cases may require transfer either to another hospital with specialized facilities, or to another department in the same hospital. 2. The level of care should not be allowed to drop during the transfer. 3. The patient requires repeated evaluation as some injuries may present late after the accident, e.g., some injuries of the spleen, retroperitoneal duodenal injuries, and subdural haematoma. - Chapter 2: Major Trauma and the Multiple-Injury Patient POINTS TO REMEMBER The f ives of maj or trauma: At the end of the major survey, detect or exclude the following five serious problems: • Airway obstruction. • Pneumothorax, open or tension • Massive haemothorax • Flail chest • Cardiac tamponade When you face a patient with severe bleeding, remember the five areas of potentially severe bleeding: • Chest • Abdomen • Pelvis • Long bone fractures • External bleeding The five causes of upper airway obstruction: • Tongue • Blood • Loose teeth or denture • Vomitus • Soft tissue edema Five main features of respiratory distress: • Tachyponea and/or dyspnoea • Use of accessory muscles of respiration • Difficult speaking • Low oxygen saturation at bedside oximetry e.g. 80% • Agitation or confusion In analyzing the causes of death in major trauma. 3 interrelated factors (hypothermia, coagulopathy and metabolic acidosis) make a vicious circle leading to a potentially fatal outcome: Hypothermia; leads to slowing of the clotting factors and coagulopathy. Warming of the patient by a favourable external temperature, blankets or the use of warm i.v. fluids is essential. Coagulopathy in turn leads to diminished tissue perfusion, exaggeration of the shock state and metabolic acidosis due to anaerobic metabolism. Chapter 3: Fluid, Electrolyte Balance and Acid-Base Regulation - CHAPTER 3 FLUID, ELECTROLYTE BALANCE AND ACID-BASE REGULATION Claude Bernard was the first to recognize that to CHAPTER CONTENTS function effectively, the body needs a stable 'milieu • Physiological considerations: interieur'. That 'milieu' is mainly water in which certain o Body water o Electrolyte metabolism inorganic salts (electrolytes) are dissolved, that keep a o Acid-base regulation constant body osmolality. A very delicate acid-base Water imbalance regulating mechanism is also crucial for life, since most o Water depletion enzymatic processes operate only within a narrow pH o Water excess range. Electrolyte imbalance Water, electrolyte, and pH imbalances rarely occur in pure form or in isolation; clinical problems are mixtures. In this chapter, for purposes of understanding and planning therapy, it was found useful to categorize clinical abnormalities. Physiological Considerations Body water: • The total body water varies from 45-75% of the body weight, depending on the body content of fat. An adult male contains 60% water; a female having more fat contains 55% water, while a newborn infant has 75% water. o Hyponatraemia o Hypematraemia o Hypokalaemia o Hyperkalaemia o Calcium imbalance Acid-base imbalance o Metabolic acidosis o Metabolic alkalosis o Respiratory acidosis o Respiratory alkalosis Practical applications o Diagnosis of imbalances o Postoperative fluid and electrolyte therapy heavy water The total body water is divided into intracellular (2/3) and extracellular (1/3) compartments. The extracellular fluid (ECF) is further subdivided into the interstitial compartment and the intravascular compartment which is the plasma. Water freely distributes through all body compartments to bring the osmolarity of all compartments into equilibrium. The sources of water in the body are either exogenous or endogenous. Exogenous water intake is provided either by drinking or ingestion of solid food. The input varies widely, but averages 2-3 litres per day, of which slightly less than half is contained in solid food. Endogenous water is released during the oxidation of carbohydrates to water and carbon dioxide, and is known as metabolic water which amounts to 350 ml water pre day. Iggy lntracellular compartment 2/3 Fig. 3.1: Distribution of body water. • Two thirds are intracellular. • One third is extracellular. Water = 60% of body wt. Intracellular = 40% of body wt. Extracellular= 20% of bodywt. Interstitial 15% Plasma 5% This total water input is normally balanced with the water output from the body. Water is lost from the body by four routes: (lungs, skin, faeces and urine). .aiiJ Chapter 3: Fluid, Electrolyte Balance and Acid-Base Regulation 1. Lungs. About 400 ml of water is lost in expired air each 24 hours and is greater with increased respiratory rate. 2. Skin. Water is lost through the skin by two mechanisms; an obligatory insensible perspiration containing virtually no sodium and an active sweating rich in sodium depending mainly on climatic conditions. In a temperate climate, the average insensible obligatory water loss is between 600-1000 ml per day. 3. Faeces. Between 60-150 ml of water are lost by this route daily and is increased with diarrhea. 4. Urine. The output of urine is under control of multiple influences, such as blood volume, hormonal and nervous factors, the most important of which is the antidiuretic hormone (ADH). The amount of water excreted in urine varies after the previous three routes have been met. The normal urinary output is approximately 1500 ml/day. A minimum urinary output of about 400 ml/day is required to excrete the end products of protein metabolism. Intracellular comparbnent Significance of serum electrolyte estimation • . Na• tells you the state of water balance, e.g., a high serum sodium indicates pure water loss. • K• tells you the patient's serum potassium status. This must be kept as close to normal as possible.. • Hco; tells you if the patient has metabolic acidosis or alkalosis. Interstilial compartment Fig. 3.2: Extracellular electrolyte levels Electrolyte metabolism: Sodium is the main extracellular cation and potassium is the main intracellular cation. The normal serum electrolyte levels (Fig. 3.2) are roughly: Cations • Anions Na+ 142 mmol/L K+ 4 mmol/L er 103 mmol/L HCO3- 25 mmol/L Under normal conditions, the number of anions must equal the number of cations to keep the electrochemical neutrality of the ECF. The main cations are sodium and potassium, while the main anions are chloride, bicarbonate, phosphates, sulphates, proteins and organic acids. Practically HCO3- and er are the anions that are measured in the laboratory. Thus, when we add the normal values for these, they are less than those of the cations. The difference is known as the anion gap, and represents the other anions that are not usually measured. The interstitial fluid content is similar to plasma but with very low protein and a slightly higher chlorides. Sodium: Sodium is the main extracellular cation. It plays a central role in maintaining blood volume. Chapter 3: Fluid, Electrolyte Balance and Acid-Base Regulation 11111111 • There ·is normally a balance between sodium intake in the diet and its output mainly in urine, some in faeces and a negligible amount in insensible perspiration. However, in hot climate, profuse sweating results in a considerable loss of sodium. • The average daily intake of sodium is 1 mmol/kg, which is about 5 gm/day, equivalent to 500 ml of isotonic 0.9% saline solution. • Sodium balance is largely controlled by regulating its output which is governed by the variation in the avidity with which the renal tubules reabsorb sodium from the glomerular filtrate and the amount of sodium excreted by the sweat glands. This is under the control of the adrenal corticoids; the most powerful conservator of sodium being aldosterone. • Obligatory reduction in sodium excretion follows surgery or trauma for a period of about 48 hours due to increased adrenocortical activity. It is inadvisable to administer large quantities of isotonic saline (0.9%) solution immediately after surgery for about two days. Potassium: • Potassium is the major intracellular cation. • Abnormalities of potassium concentration are of concern because of the risk of cardiac arrhythmias. • The normal daily potassium intake is about 1 mmol/kg, mainly in potassium-rich food such as fruit, milk and honey. • Potassium excretion is mainly in urine and almost equals the intake. A very small quantity is lost in formed faeces and still a smaller quantity in sweat. • Augmented potassium excretion follows surgery and trauma. There is a period of increased excretion of potassium by the kidneys varying directly with the degree of tissue damage. This loss is greater during the first 24 hours and lasts for about 3-4 days. So great are the reserves of potassium that, unless the patient is severely depleted at the time of operation, hypokalaemis may not reveal itself for 48 hours. Calcium • The majority of body calcium is found in bones in form of phosphate and carbonate. The remainder is present as an extracellular cation which exists in almost equal two forms: 1. Ionized free fraction , which is responsible for the biologic effects of calcium, such as the neuromuscular stability, blood coagulation and cellular enzyme processes. 2.Non-ionized protein-bound, chiefly albumin. • Determination of the plasma protein level is essential for proper analysis of the serum calcium level. A low albumin level gives a false low total serum calcium concentration and vice versa. • The ratio of ionized to non-ionized calcium is related to the PH: acidosis causes an increase in the ionized fraction, whereas alkalosis causes its decrease; respiratory alkalosis due to hyperventilation results in tetany with an apparently normal total serum calcium level. - Chapter 3: Fluid, Electrolyte Balance and Acid-Base Regulation • The normal serum level is between 8.5 and 10.5 mg/di (4.25-5.25 mEq/L or 2.2-2.5 mmol/L). • The serum calcium level is likely to be modified by vitamin D, parathormone, calcitonin and the state of renal and small bowel function. Acid-base regulation: The normal ECF pH is 7.4 ± 0.04, and most enzymatic processes operate only within a narrow pH range (7.3-7.5). Normal metabolism produces approximately 15000 mEq Hiday. Mechanisms for the regulation of body pH can be divided into three categories: • Body buffer systems (pH shock absorbers): The most important of these systems is the bicarbonate-carbonic acid ratio, which is normally 20:1. Alteration in this ratio changes the pH regardless of the absolute values of the bicarbonate and carbonic acid. A decrease in the ratio leads to increased acidity and vice versa. The bicarbonate level can be changed by metabolic factors, while carbonic acid level is subjected to alteration by respiratory factors. Alteration of one is followed automatically by a compensatory change in the other in an attempt to keep this ratio and pH constant. • Renal regulation (works in hours and days): These function to maintain body pH by: o Reabsorbing filtered bicarbonate. o Excreting 50-100 mmol of H+/day. Renal failure is associated with a state of chronic acidosis. • Respiratory regulation (works within minutes): This occurs by elimination of CO2, which is the source of carbonic acid. Since CO2 diffuses approximately 20 times more readily than 0 2, severe respiratory impairment must occur before CO2 retention occurs. Water Imbalance Water depletion (pure dehydration): Pure water depletion is rare in surgical practice. Aetiology 1. Lack of water intake. This may be due to lack of availability, difficulty to swallow or inability to swallow in comatosed patients. 2. Diabetes insipidus. 3. Increased output in fever and osmotic diuresis. Consequences: • A water deficit results in a decrease in volume of all the body fluid compartments. • Since solute content does not change, hyperosmolality results. • Osmoreceptors are stimulated, and secretion of ADH is increased. More water is reabsorbed from the distal renal tubules. Chapter 3: Fluid, Electrolyte Balance and Acid-Base Regulation &111111 Clinical features: 1. The main symptoms are intense thirst and weakness. 2. Reduced tissue turgor. 3. Oliguria with high specific gravity. Treatment: 1. An initial estimate of the magnitude of water deficit can be made from clinical data and by assuming that each 3 mmol elevation of serum sodium concentration above normal range represents a deficit of approximately one litre of body water. 2. Treatment of a water deficit requires provision of additional sodium-free water, e.g., IV 5% glucose. Water excess (water intoxication): Aetiology: Water excess often is iatrogenic, resulting from administration of electrolyte-free water. 1. The commonest cause on surgical wards is over-infusion of intravenous 5% glucose solution to postoperative patients. 2. Colorectal washouts with plain water instead of saline before colonic surgery. 3. A major component of the transurethral resection of the prostate (TURP) syndrome is the water intoxication caused by excessive uptake of water from irrigation fluid. In current practice water is replaced by glycine to overcome this problem. Consequences: • Water excess leads to an increase in the volume of all fluid compartments. Since body solute content is not altered, a state of hypo-osmolality results. • Hypothalamic osmoreceptors are inhibited, and pituitary secretion of ADH is decreased resulting in increased renal water excretion. Clinical features: • Moderate water excess is often well tolerated and asymptomatic. The only findings are: o Increased urine volume. o An increase in body weight. Pitting edema usually does not develop. o Decreased serum sodium concentration and falling haematocrit value. Marked water excess causes (serum sodium concentration is below 120 mEq/litre): o Swelling of brain cells that leads to drowsiness, weakness, and ultimately convulsions and coma (Water intoxication). o Nausea and vomiting of clear fluid are common. Treatment: • Mild water excess requires water restriction only. llllfll Chapter 3: Fluid, Electrolyte Balance and Acid-Base Regulation • Severe cases: o Induction of diuresis by mannitol. o Careful infusion of small amounts of concentrated (3%) sodium chloride. Electrolyte Imbalance Hyponatremia: 140 EC ASIC 135mean The serum concentration is 135-145 mmol/L. Hyponatraemia is a serum Na+ concentration less than 135 mmol/L. In surgical practice hyponatraemia occurs mainly hypo either as dilutional (hypervolaemic) or depletion (hypovolvaemic) hyponatraemia. Aetiology: • Dilutational hyponatraemia (hypervolaemic) hyperosmod o Excessive intake of salt free solutions e.g. dextrose 5%. o Post-operatively due to excess secretion of ADH. o Liver cirrhosis and congestive heart failure. • Depletion hyponatraemia (hypovolaemic) hypososine 125 malaise 120 1115 Seizer o Abnormal gastrointestinal losses due to persistent vomiting, diarrhoea, intestinal obstruction and intestinal fistulae. The sodium conent of most gastrointestinal secretions is nearly similar to plasma. o Loss of ECF in burns, or third space losses (peritonitis, ileus or ascites) o Excess loss of Na+ in urine as salt losing nephritis, diuretics or adrenal failure. Clinical picture and treatment: I SO Osmolars Dilutional hyponatraemia: Mo~t patients with serum Na+ concentration greater than 120 mmol/L are asymptomatic. Most symptoms of dilutional hyponatraemia are cerebral due to shift of water to the brain cells. There is agitation, disorientation, delirium, emesis, headache and seizures. Treatment: • Restrict water intake • If the hyponatraemia is severe (serum Na <120 mmo/L) or neurological symptoms are present, give hypertonic (3%) saline. • Avoid rapid correction of hyponatremia as it may lead to serious neurological disorder called central pontine myelinolysis Depletion hyponatraemia: The symptoms and signs of sodium depletion are caused by decreased ECF volume. • The eyes are sunken and the face is drawn, In infants the anterior fontanelle is depressed. The skin is dry and often wrinkled. • The tongue is coated and dry. Chapter 3: Fluid, Electrolyte Balance and Acid-Base Regulation - • Unlike the dehydration produced by loss of water only, in water and salt depletion thirst is not particularly in evidence. • Peripheral veins are contracted. Hypovolaemia results in tachycardia, orthostatic hypotension and shock. Low CVP. Urine is scanty, dark, and of a high specific gravity. Normal or slightly reduced serum sodium. Serum sodium concentration is not a measure of the total body sodium content. Treatment: Restoration of ECF volume by appropriate amounts of sodium-containing fluids such as normal saline (sodium chloride 0.9%) or Ringers lactate. Sodium Excess (hypernatraemia) Causes: 1. If patients are given an excessive amount of 0.9% saline solution intravenously during the early postoperative period, when some degree of sodium retention is to be expected. The result is an overloading of the circulation with salt and its accompanying water. 2. Hyperaldosteronism: a. Primary (Conn's syndrome) b. Secondary as in cases of liver cirrhosis 3. Cushing's syndrome (hyperadrenocorticism). Clinical features: 1. Slight puffiness of the face is the only early sign. 2. The only reliable clinical sign of total body sodium excess is oedema. 3. ·Weight gain parallels accumulation of ECF. 4. Hypertension. Serum sodium concentration is usually normal. Treatment: Sodium restriction and careful use of diuretics. K2 MEQIL Potassium Depletion (hypokalaemia) 3 1333400 MEO metaboli Alkalosis Nougadin Since serum potassium content represents a small part of total body potassium, small reductions in its serum level may reflect large body losses of potassium. Aetiology: 2 Batak 1. Excessive vomiting, e.g. pyloric stenosis, intestinal obstruction and paralytic ileus. Prolonged gastroduodenal aspiration with fluid replacement by intravenous isotonic saline solution is a frequent cause of hypokalaemia in surgical patients. 31121A It .-II Chapter 3: Fluid, Electrolyte Balance and Acid-Base Regulation 2. External alimentary fistulae. 3. Diarrhoea especially when severe as in cholera, ulcerative colitis, villous tumours of the rectum, or ileostomy dysfunction. 4. Certain types of diuretics as furosemide. 5. Alkalosis due to shift of potassium into the cells without a change in the actual body potassium content. 6. Hyperaldosteronism. Aldosterone causes potassium loss. Consequences: • Hypokalaemia raises membrane excitation potentials , making nerves and muscles less excitable. • Risk of supraventricular arrhythmias. • Potassium depleted patients are prone to develop hepatic coma if they have liver disease. Clinical features: • Most patients are asymptomatic. • Early signs of potassium depletion are vague; malaise, and weakness. The speech is slow and slurred. • Paralytic ileus and distention are seen in some hypokalaemic patients. • Muscular paresis appears only with extreme depletion. Weakness of the respiratory muscles leads to inadequate ventilation and atelectasis. • ECG reveals prolonged QT interval, depression of the ST segment, and a lowering or inversion of the T wave. U-wave is present. Treatment: • At a normal pH in the adult, the potassium deficit is calculated as follows: (4.5 - serum potassium concentration) x 100. • The required quantity of potassium is added to the infusion and distributed all over the day. It should be emphasized that potassium can be very dangerous because hyperkalaemia causes cardiac arrhythmias and asystole. It should never be injected as a bolus, Safe rules for giving potassium are: o Urine output at least 40 ml/hour. o Not more than 40 mmol added to 1 litre. o No faster than 40 mmol/hour. 75.5 Fed Potassium Excess (hyperkalaemia) Causes: of EIGA Oliguria or Anuria will be that lead to 1. Life-threatening potassium excess usually occurs only in association with renal failure and is made worse by tissue destruction or by depletion of sodium or calcium. 2. Acidosis due to shift of potassium outside the cells to the ECF Diabetic patients in whom there is reduced or absent insulin secretion are more prone to hyperkalaemia. Chapter 3: Fluid, Electrolyte Balance and Acid-Base Regulation 111111 Consequences: • Elevation of serum K to about 5 mmol/L stimulates secretion of aldosterone, which enhances excretion of potassium by the kidney. • Hyperkalaemia decreases membrane excitation potentials, making cells more excitable. If the serum potassium exceeds 7 mmol/L, intracardiac conduction is slowed and arrhythmia, bradycardia and hypotension may be followed by cardiac arrest. • The ECG is a sensitive investigation for hyperkalaemia It shows a wide QRS complex and peaked T waves. Treatment: 1. IV calcium gluconate. Calcium antagonizes potassium. 2. IV sodium bicarbonate. Alkalinization encourages intracellular shift of potassium. 3. Dextrose and insulin infusion. 10 units of regular insulin plus 20 gms of glucose. Insulin stimulates deposition of potassium with glycogen. Dextrose is added to prevent hypoglycemia. 4. If the previous measures fail, they should be followed by ion exchange resins, e.g. sodium polystyrene stilfonate, 50 gm in 70% sorbitol by mouth or enema. Repeated enemas may be performed. 5. If all the previous measures fail to lower the serum potassium, dialysis should be started. Calcium Imbalance 232m16 45EI_ Hypocalcaemia may be transient and latent, e.g., hypoparathyroidism following thyroid surgery. It is evidenced by circumoral tingling and numbness, and a positive Chvostek's sign is elicited. Symptomatic hypocalcaemia develops in established permanent hypoparathyroidism, acute pancreatitis and acute alkalosis, e.g., hyperventilation. The clinical manifestations are neuromuscular: hyperactive deep tendon reflexes, muscle and abdominal cramps, carpopedal spasm and rarely convulsions. ECG shows prolonged QT interval. Treatment is directed to correct the underlying cause. Intravenous calcium gluconate or calcium chloride is given for the acute problem. Chronic hypocalcaemia is treated by vitamin D, oral calcium supplements and aluminum hydroxide gels to bind phosphate in the intestine. Acid-Base Imbalance t Metabolic causes of acid-base disturbances are indicated by changes in the standard bicarbonate level and base excess or deficit. Respiratory causes of acid-base disturbances are indicated by changes in the PCO2 and PO2. Metabolic acidosis: - This is a condition where there is a deficit of base or an excess of any acid other than H2CO3. - - - ind - Chapter 3: Fluid, Electrolyte Balance and Acid-Base Regulation Aetiology: 1. Overproduction of organic acids - a. Diabetic ketoacidosis. Retoacidose b. Lactic acidosis of sepsis and shock. - 2. Renal failure (acute and chronic) - insulis 3. Excessive loss of bicarbonate - a. Diarrhea - b. Pancreatic or small intestinal fistula. - c. Ureterosigmoidostomy.Agira them - 4. Ingestion of ethylene glycol or methanol. ora give give Alkali - - Pathology: The standard bicarbonate level is lowered and there is a base deficit. Compensation: • Respiratory. Metabolic acidosis almost always is at least partially compensated by stimulation of respiratory activity. This stimulation results in washing out the CO2 resulting in a decrease in PCO2 bringing the HCO3-/PCO2 ratio and the pH back toward normal. • Renal. Later, renal compensation occurs. Renal excretion of acid increases. This effect is important in chronically acidotic patients with good renal function. Clinical features: Increased rate and depth of breathing (Kussmaul's respiration). - - Treatment: • Mild to moderate acidosis. Therapy should be directed at the underlying cause, e.g., restoration of adequate tissue perfusion. - • More severe acidosis: (pH 7.3 or serum bicarbonate below 15 mEq/litre). IV bicarbonate. The required amount of bicarbonate = Body weight (Kg) X 0.3 X base I deficit. - - - - Metabolic Alkalosis e - ② This means a rise in the pH due to accumulation of HCO 3-. & & & Aetiology: 1. Gastrointestinal losses of H due vomiting or removal (suction) of gastric secretion. This is the most common cause and is usually seen in patients with pyloric stenosis. - - - - 2. H+ movement into the cells associated with= hypokalaemia. Intracellular potassium moves out of the cells to compensate for extracellular hypokalaemia, and H+ moves intracellularly to preserve electroneutrality. This movement results in extracellular alkalosis and a paradoxical intracellular acidosis. Replacement of potassium reverses the process and corrects alkalosis. Chapter 3: Fluid, Electrolyte Balance and Acid-Base Regulation 3. Bicarbonate retention a. NaHCO3 administration. b. Milk-alkali syndrome. Compensation: Respiratory inhibition raises PCO2. Compensation is limited by the normal hypoxic respiratory drive when PO2 reaches 50 mmHg. Clinical features: The most striking feature of severe alkalosis is Cheyne-Stokes' respiration with periods of apnea. Tetany occasionally occurs. Treatment: 1. In all instances of metabolic alkalosis caused by loss of gastric juice, replacement of chloride is essential to successful therapy. Administration of saline solution is sufficient therapy in mild metabolic alkalosis without hypokalaemia, since the kidney completes the job of correcting acid-base balance by retaining chloride and excreting sodium along with excess bicarbonate. Concomitant hypokalaemia is treated by IV infusion of potassium. 2. In severe metabolic alkalosis not responding to saline or potassium chloride alone, it may be necessary to give IV ammonium chloride or hydrogen chloride very slowly. 3. Tetany is treated by slow IV administration of 10 ml calcium gluconate. Respiratory Acidosis A fall in pH associated with a rise in PCO2 is called respiratory acidosis. Respiratory acidosis is always associated with hypoxia. This combination is life-threatening since the rising PCO2 eventually results in respiratory depression (CO2 narcosis), with attendant worsening of the hypoxia. Renal compensatory mechanisms are too slow to affect the outcome significantly. Aetiology: Hypoventilation: 1. Inhibition of respiratory drive a. Drugs as opiates or anaesthetics. b. CNS lesions. 2. Disorders of respiratory muscles or the chest wall a. Muscle weakness as in myasthenia or poliomyelitis. b. Morbid obesity. C. Flail chest. 3. Other disorders of ventilation a. Obstructive pulmonary disease. b. Pulmonary oedema. BJIIII - Chapter 3: Fluid, Electrolyte Balance and Acid-Base Regulation Compensation: In acute respiratory acidosis, the serum bicarbonate level may not be elevated since renal compensatory mechanisms have not had enough time to act. In chronic respiratory acidosis serum bicarbonate concentration is elevated. Clinical features: Restlessness. Cyanosis. Hypertension and tachycardia in the immediate postoperative period (postoperative pain also causes hypertension and tachycardia). Treatment: Mechanical ventilation is usually required. Respiratory Alkalosis Respiratory alkalosis is a condition where carbon dioxide tension in the arterial blood (PC02) is below the normal range and the pH is increased. Aetiology: It results from hyperventilation and is seen in: 1. Hysteria. 2. Hyperpyrexia. 3. In patients who are hyperventilated by a mechanical ventilator. Compensation: Increased renal excretion of bicarbonate but is usually inadequate. Clinical features: In most clinical situations respiratory alkalosis is short-lived and well tolerated. When hyperventilation stops, carbonic acid concentration is rapidly restored , and pH returns to normal. Reduced ionized calcium may manifest by paraesthesias in the extremities and carpopedal spasm. In severe cases, respiratory arrest follows. Treatment: When hysteria is the basis for hyperventilation, the patient is instructed to breathe into a paper bag. · Other situations may call for the addition of small amounts of carbon dioxide to the inspired gas mixture. Table (3.1) depicts the differences between the various types of acidosis and alkalosis. Chapter 3: Fluid, Electrolyte Balance and Acid-Base Regulation - Table 3.1: Differences between the various types of acidosis and alkalosis Defect Met. acidosis Met. alkalosis Res. acidosis Res. alkalosis Common causes • Retention of fixed acids. • Loss of base HCO3· • Loss of fixed acids • Gain of base HCO3· • Retention of CO2 (hypoventilation) • • • • • • Excessive loss of CO 2 (hyperventilation} Diabetes, uraemia Increased lactic acid Diarrhea Small bowel fistulae Vomiting, pyloric stenosis Bicarbonate/carbonic acid ratio (20/1) Reduced Elevated • Depression of respiratory centre • Obstructive pulmonary disease Reduced • Hyperventilation Elevated Compensation • Pulmonary (rapid}: increased rate and depth of breathing. • Renal (slow) • Pulmonary (rapid), reduced rate and depth of breathing. • Renal (slow) • Renal: retention of HCO3·, excretion of H• • Chlorides: shift into red blood cells • Renal excretion of Hco3· and retention of H+ Table (3.2): Depicts arterial blood gases (ABGs) in different types of acid-base disturbances. P02 is the partial pressure of oxygen, PC02 is the partial pressure of carbon dioxide. Bicarbonate (HC03·) and base excess or deficit. Normal Met. acidosis Met. alkalosis Res. acidosis Res. alkalosis PC02 36-44 mm Hg HCQ3· 22-26 mmol/L Base Reduced (compensatory respiratory washout} Reduced Deficit Elevated Excess Reduced Elevated (compensatory respiratory retention) Elevated Excess Normal Reduced Elevation is delayed (compensatory renal retention} Reduction is delayed (compensatory renal excretion} pH 7.367.44 Reduced P02 80-110 mm Hg Normal Elevated Reduced Reduced Elevated Deficit Practical Applications Postoperative fluid and electrolyte therapy: In prescribing fluid regimens for postoperative patients, three points are considered: 1. Basal requirements. 2. Pre-existing dehydration, electrolytes loss and acid-base disturbances. 3. Continuing abnormal losses over and above the basal requirements. The daily requirements of water and electrolytes in an adult are: o Water 35 ml/kg o Sodium 1 mmol/kg o Potassium 1 mmol/kg - Chapter 3: Fluid, Electrolyte Balance and Acid-Base Regulation The usual daily postoperative fluids for uncomplicated surgery in an adult: • Three litres of fluids = 6 bottles. Add 200 ml per day for each 1°c rise in body temperature. • 500 ml saline (0.9% sodium chloride) provides the daily requirements of sodium and chloride. • The remaining volume requirement (2.5 L = 5 bottles) is given as 5% dextrose (glucose). • Potassium supplements are given after 48 hours. Potassium chloride is added to the solutions. as a In loading dose a gie trace elements Vitamins Chapter 4: Acute Haemorrhage and Blood Transfusion CHAPTER4 ACUTE HAEMORRHAGE AND BLOOD TRANSFUSION CHAPTER CONTENTS Classification of haemorrhage Acute haemorrhage causes loss of both circulating blood volume and oxygen carrying capacity. The common causes include penetrating and blunt trauma, gastrointestinal bleeding, and obstetrical bleeding. Haemorrhage may be classified according to Site • External. Bleeding is visible as it occurs through skin wounds or from a body orifice as in epistaxis. • Internal o In body cavities, e.g., haemoperitoneum and haemothorax. o Interstitial, e.g., fracture haematoma. Type of disrupted vessel • Arterial. Blood is bright red and comes in pulsatile jets. • Venous. Blood is dark red and comes in a steady flow. • Capillary. Bleeding occurs as diffuse ooze of bright red blood. Timing in relation to trauma: • Classification of haemorrhage • Pathophysiological response to haemorrhage • Clinical picture of haemorrhage • Treatment of haemorrhage • Blood transfusion o Collection & storage of blood o Blood products o Possible complications o Alternatives to homologous blood transfusion Haemorrhage is classified according to: • Site: External or internal. • Type of disrupted vessel: Arterial, venous or capillary. • Timing: Primary, reactionary or secondary. • Aetiology: Traumatic, pathological or spontaneous. Common causes of severe haemorrhage: • Trauma: Splenic or liver injury, haemothorax, pelvis fracture • Major surgery • Bleeding oesophageal varices • Bleeding duodenal ulcer • Ruptured aortic aneurysm • Pre and postpartum haemorrhage Ruptured ectopic pregnancy. Body response aims to: • Stop bleeding • Maintain effective blood volume. This response is based on neural and endocrinal mechanisms. • Primary haemorrhage occurs at the time of trauma. • Reactionary haemorrhage occurs within 24 hours after trauma. As the blood pressure rises due to correction of hypovolaemia, an insecure ligature slips or a clot is dislodged. • Secondary haemorrhage occurs one to two weeks after trauma due to infection eroding a vessel wall, e.g. after haemorrhoidectomy. It can be fatal if a large artery is involved, e.g., the carotid after sloughing of the skin flaps of a radical neck dissection. Aetiology • Traumatic, which might be accidental or iatrogenic. • Pathological o Atherosclerotic, e.g., ruptured aortic aneurysm. o Inflammatory, e.g., bleeding peptic ulcer. liJIII - Chapter 4: Acute Haemorrhage and Blood Transfusion o Neoplastic, e.g., haematuria in renal cancer. • Bleeding diathesis can increase the amount of traumatic and pathological bleeding, or cause bleeding with little or no trauma (spontaneous haemorrhage). Pathophysiological response to haemorrhage The pathophysiological response to haemorrhage has two aims 1. Stopping the bleeding • Vasoconstriction and retraction of the intima of the injured vessel. • Platelet plug. • Blood clotting. , -- Capillary · Pressure Capillary refill +-+ heart rate Arteriolar constriction Constriction -venous +-+ contractillty +-+ TPR I++ Aldosterone Venous Arteriolar constriction ++ Na reabsorption ++ Blood volume capacitance ++ Arterial Prossuro towards normal ++ Arterial Pressure towards normal Fig. 4.1. Main compensatory mechanisms for haemorrhage. 2. Maintaining effective circulatory volume and perfusion of critical tissues (brain and heart), at the expense of less critical tissues (skin, skeletal muscle and splanchnic area). This is achieved by neural and endocrine factors (Fig. 4.1 ). A. Neural factors. A sympathoadrenal discharge develops due to decrease in stimulation of arterial baroreceptors (aortic arch and carotid sinus) and atrial stretch receptors leading to reduction of the normal inhibitory discharge in the vagus and glossopharyngeal nerves on the vasomotor centre with consequent stimulation of the sympathetic system. The effects include • Constriction of veins, which normally contain two-thirds of the blood volume, displaces blood from the capacitance side of the circulation into the heart. • Constriction of arterioles raises the peripheral resistance but this is not uniform. It involves mainly the arterioles of the skin, skeletal muscle, and splanchnic area. Perfusion of the heart and brain is maintained because heir metabolic needs override the alpha-adrenergic vasoconstrictor discharge. • Increased rate and strength of cardiac contraction. Chapter 4: Acute Haemorrhage and Blood Transfusion 1111111111 B. Endocrine factors • Catecholamine discharge occurs from the adrenal medulla and from the nerve endings throughout the autonomic nervous system. They increase the heart rate and myocardial contraction and cause constriction of the arterioles of the skin, kidney and viscera. ones hormone and glucagon are As cortisol, stress growth • The metabolic hormones ACTH, increased. Insulin release is inhibited by adrenaline and noradrenaline. • The renin-angiotensin aldosterone system. The juxtaglomerular cells of the afferent renal arterioles secrete renin in response to renal hypoperfusion. Renin splits angiotensinogen to angiotensin I, which is converted to angiotensin II by a converting enzyme in the lung. Angiotensin II is a powerful vasoconstrictor and stimulates sodium and water retention by a direct action on the kidney as well as indirectly through release of aldosterone from the zona glomerulosa of the Intravasal adrenal cortex. Angiotensin-mediated vasoconstriction takes some 20 minutes to occur, whereas baroreceptor-vasoconstriction occurs within seconds. Tintin now ADH (vasopressin). Blood loss greater than 10% stimulates ADH release. ADH increases the permeatJility of the renal collecting tubules allowing water absorption into the hypertonic renal medu~ary interstitium. With severe haemorrhage high levels of ADH also cause vasoconstriction. C. Transcapiilary refill. Reduction of blood volume and constriction of arterioles causes a fall in capillary hydrostatic pressure and promotes movement of fluid from the interstitium into the capillaries, resulting in increased blood volume. • If ovulatory compensationphase a spasmof changes celldistressphase Capillaryrefill Clinical picture of haemorrhage decompensation irreversible failure The manifestations depend upon the amount of blood loss. Its rate and on cardiovascular reserve. Thus, loss of only 500 ml of blood may cause hypotension in a patient with coronary artery disease, whereas in a healthy young adult, losses greater than 1500 ml may not lower systolic pressure initially. The following are the clinical manifestations of hypovolaemia. Symptoms • Weakness and fainting especially when standing. • The patient feels cold and thirsty. Signs • The patient looks tired. With decreasing cerebral perfusion, the mental status may vary from anxious to drowsy but the patient usually remains al.ert. • Pulse and blood pressure. With mild blood loss (less than 500 ml), pulse and blood pressure may remain normal thanks to the efficient compensatory mechanisms. With more blood loss, tachycardia develops but the blood pressure remains stable. With further blood loss, however, the compensatory mechanisms can no longer maintain the blood pressure and progressive hypotension develops (Table 4.1 ). • Pulse pressure (PP) decreases leading to a thready pulse. • Respiratory rate. Tachypn~a and air hunger. • Hypothermia, which predisposes to coagulopathy and should be avoided. IIIIIIII Chapter 4: Acute Haemorrhage and Blood Transfusion • Skin becomes pale, cold and sweaty with slow capillary refill and collapsed veins. • Oliguria results due to diminished renal perfusion. Table 4.1. Clinical parameters in different classes of haemorrhage. - - -- -- - - - -C -la_s_s_l Blood loss (in 70 Kg person) 15- 30% (7501500 ml) (1500-2000 ml) Normal to anxious Anxious to restless Aggressive to drowsy Drowsy to unconscious Skin Normal Pale and cold Pale and colder Pale and very cold Capillary refill Normal >2 sec. >2 sec >2 sec undetectable Pulse/minute <100 100-120 100-140 >140 - Systolic Normal Normal (supine) Low Low - Diastolic Normal Raised Low Low - Pulse pressure Normal Low Low Low 14 -20 20-30 30- 35 >35 >30 20-30 10-20 0-10 Mental status Up to 15% (750 ml) 30-40% >40% (2000 ml) Blood pressure Respiratory rate Urine (ml/h) Estimating blood loss Blood volume is estimated as 70 ml/Kg in adults and 80 ml/Kg in children. In any patient with haemorrhage, it is of importance to have a rough estimate of the amount of blood loss determined from the following. • Clinical data. Four classes of haemorrhage are recognized based on clinical changes in haemodynamic parameters and indices of tissue perfusion (Table 4.1 ). This table provides only general guidance. • Type of injury. The haematoma around a closed fracture of the tibia may contain 5001500 ml of blood, that around a fractured shaft of femur, 500-2000 ml; that in a fractured pelvis, 2000-3000 ml. • Blood loss at operation is the sum of the amount in the suction reservoir and the amount mopped up by the swabs, the latter is calculated as the difference in swab weight after and before operation multiplied by a correction factor of 1.5-2 depending on the magnitude of the operation. Investigations • Complete blood picture, including haematocrit. The initial haematocrit value is often normal (RBCs and plasma are lost in the same ratio). Some 4-6 hours later, serial haematocrits will show a reduction. Haemodilution is caused by movement of interstitial fluid into the circulation and because of crystalloid replacement of lost blood. • Coagulation profile. • Cross matching. Treatment of haemorrhage 1. Stop haemorrhage. First-aid treatment is by packing, pressure, and position. A skin wound is covered by a dressing, and pressure is applied manually, by a 1.5 b4 5 Crystalloid Chapter 4: Acute Haemorrhage and Blood Transfusion - sphygmomanometer cuff or by a bandage. Tourniquets are contraindicated because of complications unless the limb is going to be amputated. Elevation of the limb above the heart level stops venous and decreases arterial bleeding. Other examples of first aid treatment include the pneumatic anti-shock garment (PASG), which can tamponade lower limb, pelvic and abdominal haemorrhage. The garment increases peripheral resistance and so raises the blood pressure. Another example is balloon tamponade of haemorrhage from oesophageal varices. The definitive management depends upon the cause of bleeding. 2. Restore blood volume. A large bore cannula is inserted in a large peripheral vein, preferably in the upper limb, or by a cut down on the long saphenous vein, if necessary. Volume replacement depends on the class of the haemorrhage. Class II • The deficit is estimated at 15-30% (750-1500 ml/70 kg). • The replacement solution is lactated Ringer's. • The amount is 3 times the estimated deficit (-3 L). The 3: 1 rule serves to replenish the interstitial fluid volume when the crystalloid diffuses out of the capillaries. • Administration. Two litres are given as a bolus and the response is monitored. If there is definite improvement: the remaining litre is given more slowly followed by the maintenance requirements and continued observations (a haematocrit <30 requires blood transfusion). If there is moderate improvement, the possibilities are inadequate replacement, continuing haemorrhage or myocardial insufficiency. Cardiac tamponade and tension pneumothorax must be excluded. Blood transfusion is started if bleeding is still active. Cardiac Class Ill and IV means Aorns Aneurysm failure • The management is as for class II but these patients need blood transfusion. The initial volume of transfused blood is that of the estimated deficit (1500-2000 ml). • Failure to improve and a rising CVP indicate tension pneumothorax, cardiac tamponade, or cardiac failure. If these are excluded and the patient does not improve, major thoracic, abdominal, or pelvic injury is usually present and calls for immediate operation to control the bleeding. Clean blood in the thorax or abdomen can be aspirated, anticoagulated and then transfused back into the patient (autotransfusion), if a cell-saver is available. • Transfusion should continue until the haematocrit has reached 30%, the urine output 50 ml/hour, and the CVP has risen to the upper half of the normal range. 3. Optimize oxygen delivery. Forty percent oxygen is given for class II haemorrhage and 100% for classes Ill and IV. Intubation and mechanical ventilation and the use of inotropes (dopamine and dobutamine), vasodilators and vasopressors may be 40 necessary if raising oxygen carrying capacity by blood transfusion does not improve lass oxygen delivery. 01 31 4. Monitoring is important to prevent the clinical sequelae and complications of hypovolaemic shock, i.e., cardiac arrest, adult respiratory distress syndrome (ARDS), acute renal failure, GIT dysfunction with stress bleeding, and disseminated intravascular coagulation (DIC). 2 What to monitor? • The parameters in Table 4.1 suffice if the patient is fit and responds quickly to bolus infusion of 2 litres of Ringers lactate solution. A Foley catheter is necessary to morphine is fine body core temperature 25 normally Any increase 111111!1 Chapter 4: Acute Haemorrhage and Blood Transfusion Perfusion
