Shock and trauma

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CHAPTER 4 Shock and trauma

Shock

Shock is defined as an abnormality of the circulation that causes inadequate organ perfusion and oxygenation. Five types of shock may be encountered in surgical practice: hypovolaemic, septic, cardiogenic, neurogenic and anaphylactic.

Hypovolaemic shock

This is due to decreased circulating blood volume.

Causes

• haemorrhage, e.g. trauma, haematemesis, ruptured aortic aneurysm

• dehydration, e.g. severe vomiting or diarrhoea, third space loss in inflammatory conditions

• burns resulting in massive loss of serum.

Classification

The blood volume of a 70 kg man is approximately 5 L or 80 mL/kg. Hypovolaemic shock can be divided into four categories, depending on the amount lost:

I. <750 mL or <15%

II. 750–1500 mL or 15–30%

III. 1500–2000 mL or 30–40%

IV. >2000 mL or >40%.

Symptoms and signs

The symptoms and signs relate to the amount of blood lost:

I. Minimal symptoms

II. Tachycardia >100, tachypnoea, decreased pulse pressure, pale, sweaty, cold peripheries

III. Classic symptoms of shock – tachycardia >120, hypotension, tachypnoea, pallor, cold peripheries, decreased conscious level, oliguria

IV. Immediate threat to life – tachycardia >140, hypotension (unobtainable diastolic), pallor, cold peripheries, unconscious (>50%), anuria.

Treatment

Shock is a surgical emergency and needs rapid treatment.

1. Ensure an adequate airway. Deliver 100% oxygen by mask. If comatose, intubate.

2. Keep the patient recumbent and elevate the foot of the bed.

3. Establish vascular access with two large-bore intravenous catheters – ideally in the antecubital fossa. If the cause of shock is haemorrhage, take blood for cross-matching. Also take blood for haemoglobin, haematocrit and U&Es. Restore circulating volume with crystalloid initially and with plasma expanders or blood as indicated.

4. Compression of any obvious external haemorrhage, i.e. stab wound to the groin.

5. Insert a central venous line to monitor CVP and to assess the response to fluid administration.

6. Insert a urinary catheter to monitor urinary output.

7. Establish basic observations of temperature, pulse, BP, respiratory rate and level of consciousness and urinary output.

8. The underlying cause of the shock should be ascertained and definitive treatment planned. Failure of resuscitation may be due to persistent massive haemorrhage. Surgical intervention is often necessary.

Septic shock

Septic shock is part of the systemic inflammatory response syndrome (SIRS). Sepsis is defined as SIRS with a confirmed source of infection. Septic shock is defined as hypotension and hypoperfusion despite adequate fluid resuscitation. Septic shock is uncommon in trauma unless there has been a delay in presentation.

Causes

Septic shock is due to the release of a number of pro-inflammatory mediators such as IL-1, IL-6, TNF-α, PAF and the eicosanoids; and as a result of bacterial endotoxins (lipopolysaccharides). Septic shock is usually due to Gram-negative organisms such as E. coli, Klebsiella and pseudomonas, although peptidoglycans and teichoic acids in Gram-positive bacteria can also have similar effects. The pathophysiology underlying shock in septic patients includes:

• peripheral vasodilation

• ↑ vascular permeability (third space loss)

• peripheral arteriovenous shunting

• myocardial depression due to toxic effects on heart

• uncoupling of oxidative phosphorylation and anaerobic respiration leading to severe metabolic acidosis.

Symptoms and signs

There may be an obvious source of infection, together with a predisposing condition. The patient may be confused and restless; initially the skin is hot and flushed and the pulse characteristically ‘bounding’. Vasoconstriction and the classic signs of shock may develop later.

Treatment

This is urgent and involves resuscitation, identification of the source of sepsis, appropriate antibiotic therapy and any necessary surgery to eradicate the focus of infection.

1. Ensure adequate airway and ventilation.

2. Restore circulating volume with plasma expanders while monitoring the venous pressure and urine output.

3. Obtain FBC, U&E, LFTs, clotting screen, ABG, serum lactate, cultures of blood, sputum, urine and any drainage fluid.

4. Commence intravenous antibiotics. This will depend on a number of factors. These include:

— Site of sepsis – from the patient history and clinical examination, a best guess site of sepsis can usually be ascertained, i.e. GI, respiratory, urinary and secondary to intravascular lines.

— Previous antibiotics – a patient who develops septic shock after prophylactic antibiotics is likely to have infection from a resistant organism and thus use of a different antibiotic is essential.

— Length of time in hospital – organisms in the community and nosocomial organisms differ greatly; a patient admitted from the community with septic shock from a respiratory infection will require different antibiotics to a patient from ITU who has been in hospital for 4 weeks.

— Local resistance – depending on whether the patient is ward-based or on ITU, the likely infecting organism and likely antibiotic resistance will differ. This is also true from hospital to hospital. In these situations it is best to consult the on-call microbiologist. They will be able to give advice on the likely organisms responsible and on the most appropriate antibiotic therapy.

5. Carry out appropriate surgical intervention, e.g. drainage of abscess, peritoneal lavage.

6. Further supportive measures may be required, e.g. inotropic agents, ventilation.

Complications

Sepsis and septic shock can progress to MODS (multi-organ dysfunction syndrome) and MOFS (multi-organ failure syndrome). Patients with MODS often present with sequential failure of organs, lung – liver – intestine – kidney; this may present as ARDS, abnormal LFTs, ileus and renal failure. With continued illness, organ dysfunction progresses to organ failure. Mortality with one-organ failure is around 30%. This rises to 100% with four-organ failure.

Cardiogenic shock

Cardiogenic shock or ‘pump failure’ is due to a loss of myocardial contractility.

Causes

These can be divided into cardiac compressive, cardiac obstructive or functional. All lead to problems with myocardial function and an inadequate cardiac output.

• Compressive – external forces compress the heart and great vessels leading to impairment of diastolic filling, a decrease in stroke volume and consequent hypotension. Causes include cardiac tamponade, positive pressure ventilation, tension pneumothorax and abdominal compartment syndrome.

• Obstructive – occurs when intravascular obstruction, excessive stiffness of arterial walls and microvascular blockage places an undue stress on the heart. It may be right- or left-sided. Tension pneumothorax is the commonest traumatic cause but other causes include valvular stenosis, PE and ARDS.

• Functional – the heart itself is not functioning efficiently. This may be due to arrhythmias or impaired muscle function after contusion or infarction.

Symptoms and signs

The traumatic causes will be discussed later in the chapter. Cardiac causes may present with chest pain and collapse. There may be a past history of cardiac problems or presence of risk factors, i.e. diabetes. Patients may be dyspnoeic with signs of pulmonary oedema. The patient may also display the classic signs of shock, i.e. pale, clammy, tachycardia, hypotension. Pulmonary embolism may present similarly (→ Ch. 5).

Investigations

Urgent investigations include portable CXR, FBC, U&E, cardiac enzymes, D-dimers, ABGs, ECG, CXR.

Neurogenic shock

Neurogenic shock is due to impaired descending sympathetic pathways in the spinal cord; this results in loss of vasomotor tone and sympathetic innervation to the heart. This leads to pooling of blood in the lower limbs. Although neurogenic shock can occur with spinal injury, it is not synonymous with spinal shock; this refers to the flaccidity and areflexia seen after a spinal injury. Neurogenic shock also occurs from certain nervous stimuli, i.e. fright – this leads to a sudden dilation of the splanchnic vessels and a bradycardia – the transient hypotension may lead to collapse.

Anaphylactic shock

Anaphylactic shock is a type I hypersensitivity reaction occurring in response to a previously sensitized antigen. Shock occurs as a result of vasodilation and increased vascular permeability. In surgical practice this may follow administration of drugs or radiological dyes. In the community it may follow wasp or bee stings or ingestion of certain foods, i.e. peanuts.

Trauma

Trauma is the main cause of death in people under the age of 35 years. It constitutes up to 20% of surgical admissions. Mortality can be greatly reduced by appropriate handling of the injured in the following three settings:

1. Emergency medical teams capable of going to the scene of an accident and providing the necessary first aid

2. A transportation system capable of rapid transport to a specified trauma centre

3. A trauma centre with trained personnel who are capable of rapidly assessing the injuries with facilities capable of handling a large number of trauma cases with trained teams.

Initial assessment of the trauma patient

Pre-hospital care

In the pre-hospital phase, the same priorities exist in terms of ABCs; there is particular emphasis on airway control, control of external bleeding and immobilization. The key is to limit time on the scene and to transfer the patient to the nearest appropriate hospital. Communication with the hospital to allow mobilization of the trauma team is vital.

Major incident triage

Triage is the process of defining the most serious injuries in a mass casualty situation and attempting to have the greatest benefit with the given resources. Multiple casualties implies a number of wounded patients but not sufficient to exceed the ability of the hospital to offer care. Mass casualties implies that the number of injured will exceed the facility’s ability to treat all patients and those with the greatest chance of survival are treated first. In the military, colour categories are applied to the wounded and indicate immediate, urgent or delayed treatment, dead or expectant.

Trauma scoring systems

Scoring systems in trauma can be divided into physiological scores and are based on a patient’s response to injury (e.g. GCS and Revised Trauma Score); anatomical scores based on the injury that has occurred (e.g. Injury Severity Score and Liver Injury Scale); and outcome systems based on the result after recovery (e.g. GCS). Scoring systems are useful for a number of reasons such as facilitating triage, organizing trauma systems and to allow accurate comparisons between populations and treatment methods.

Initial assessment and resuscitation

This should follow ATLS (Advanced Trauma Life Support) guidelines. Initial assessment is divided into a primary survey where patients are assessed and their treatment priorities established based on their injuries, vital signs and mechanism of injury. This is followed by a secondary survey, which does not begin until the primary survey is completed, resuscitation is well established and the patient has normal vital signs.

Primary survey

This process constitutes the ABCDE protocol of ATLS and aims to rapidly identify immediately life-threatening injuries in a sequence in which the most rapidly fatal conditions are diagnosed first (i.e. airway obstruction will be fatal before splenic injury). The ABCDE of the primary survey is below.

ABCDE of emergency management:

• A = Airway and cervical spine control – Ensure a clear airway. The mouth and upper airway should be inspected for foreign bodies; these should be removed. In an unconscious patient the initial airway management may be a simple chin lift or jaw thrust; if this is unsuccessful in maintaining an airway then an oral (Guedel) or nasopharyngeal airway can be used. If these fail to maintain the airway then intubation will be necessary. In patients with severe maxillofacial trauma a surgical airway such as jet insufflation (needle cricothyroidotomy) or surgical cricothyroidotomy may be needed. Emergency tracheostomy has no role as an emergency airway manoeuvre.

• B = Breathing – Check for chest movements, asymmetry of movements, respiratory rate, abrasions or bruising over the chest, cyanosis, use of accessory muscles, distension of neck veins. Examine the chest for pain, crepitations (indicating subcutaneous emphysema), auscultation, percussion and palpation of the trachea. Needle decompression may be needed for tension pneumothorax and a chest drain may be required for pneumothorax or haemothorax.

• C = Circulation and haemorrhage control – i.v. access should be gained with two large bore cannula (12–14G) in the antecubital fossa. Two litres (L) of Hartmann’s solution should be rapidly infused. Alternative sites for vascular access include central veins, i.e. subclavian or femoral (internal jugular can be difficult to use due to the presence of C-spine collars), cut-down onto the long saphenous vein and intraosseous infusion (children only). Obvious haemorrhage can be treated with compression dressings. Tourniquets are not indicated.

• D = Disability – In the primary survey a rapid assessment of neurological status is made. This includes assessment of pupillary size and level of consciousness. The level of consciousness can be remembered by the mnemonic AVPU:

— V = responds to Vocal stimuli

— P = responds to Painful stimuli

— U = Unresponsive.

• E = Exposure and environmental control – The patient should be fully undressed and examined from head to toe (secondary survey). The patient’s temperature must be monitored and hypothermia prevented by covering with warming blankets and the use of warmed i.v. fluids.

During the primary survey and in tandem with examining the patient, certain adjuncts are used, including ECG, pulse oximetry, BP and respiratory rate, insertion of NG tube and urinary catheter (as required); also the patient is provided with adequate analgesia.

Secondary survey

The secondary survey is a head-to-toe evaluation of the trauma patient, i.e. a complete history and physical examination, including a reassessment of all vital signs. Each area of the body should be completely examined. A full neurological examination is carried out including a GCS (Glasgow Coma Score) determination (Table 4.1).

TABLE 4.1 Glasgow Coma Scale (GCS)

Responses	Score
Eye-opening response
Spontaneous	4
To voice	3
To pain	2
None	1
Best verbal response
Orientated	5
Confused	4
Inappropriate speech	3
Incomprehensible speech	2
None	1
Best motor response
Obeys commands	6
Localizes pain	5
Withdraws to pain	4
Flexion to pain	3
Extension to pain	2
None	1
Total	3–15

A score of 3 indicates a severe injury with a poor prognosis. A score of 13–15 indicates minor injury with a good prognosis.

History

This is obtained from the patient (if possible), ambulance staff or other witnesses. Ascertain the time of the accident, the type of accident, the conscious level of the patient at the time of the accident and any change since; any blood loss, details of drugs administered at the scene of accident, previous medical history including drugs and allergies, details of food, alcohol and drug intake. In road-traffic accidents (RTAs), details of the patient’s position in the car, speed, use of airbags/seat belts and degree of damage to the car should be obtained. A mnemonic to help remember this is to take an AMPLE history:

• Medications

• Previous illnesses

• Events surrounding injury.

Examination

An initial rapid preliminary examination will have been made during the primary survey. A full examination is carried out during the secondary survey looking for head injuries, maxillofacial injuries, cervical spine injuries, chest injuries, abdominal and perineal injuries, musculoskeletal injuries, and neurological trauma. Typical injuries include:

• Frontal impact – injuries to diaphragm, cervical spine, flail chest, myocardial contusion, pneumothorax, TRA, ruptured liver and spleen, possible dislocation of hip or knee

• Side impact – injuries to cervical spine, flail chest, pneumothorax, TRA, diaphragmatic tear, ruptured liver, ruptured spleen, ruptured kidney, fractured pelvis or acetabulum

• Rear impact – cervical spine injury

• Pedestrian – head injury, TRA, abdominal visceral injury, fractured lower limb and pelvis

• Fall from a height – calcaneal fracture, tibial plateau fracture, pelvic or acetabular fracture, lumbar spine compression fracture, TRA, pneumothorax, head injury.

Investigations

The timing of the investigations depends on the clinical state of the patient. These include: blood grouping and cross-match, FBC, U&E, amylase, LFT, glucose, β-HCG (in women of child-bearing age) arterial blood gas. X-rays in the primary survey include chest and pelvis X-ray. FAST (Focused Abdominal Sonography for Trauma) is an imaging modality often performed during the primary survey to identify an abdominal source of bleeding in a hypotensive patient. All other X-rays, CT, contrast studies, etc. are obtained depending on the stability of the patient and the presence of other injuries. As a rule, these would be obtained as part of the secondary survey. Examples include: spinal X-rays in suspected spinal injury, CT head in patients with head trauma (can often include cervical spine views), CT abdomen and chest in suspected abdominal/thoracic trauma in patients who are haemodynamically stable. Urethrography/cystography in patients with suspected urethral or bladder injury.

Head injury (→ Ch. 18)

Primary brain damage occurring at the time of injury cannot be repaired. Management should be aimed at preventing secondary injury.

Management

The management of specific head injury is dealt with in the section on Neurosurgery (→ Ch. 18) but the basic principles are outlined here as far as trauma management is concerned.

Treat hypoxia, hypercapnia, hypovolaemic shock, and anaemia to prevent further neurological deterioration. Primary neurological management is identification and rapid treatment of localized lesions and intracranial haemorrhage, cerebral debridement and prevention of raised ICP.

Hypotension in adults is not due to intracranial blood loss. However, in children, significant blood loss can occur in head injuries and can be responsible for hypotension. The scalp should be examined for lacerations and boggy wounds. Observation should be made for bleeding and CSF leakage from the ear and nose. The cranial nerves should be checked and the limbs examined. Assessment of head injured patients include skull X-rays and CT scan; indications for these are detailed in Chapter 18.

Immediate management depends on severity. The presence of abnormal pupillary reflexes, asymmetrical motor signs or deteriorating level of consciousness is an immediate indication for treatment.

Immediate measures:

• Ventilate with 100% oxygen and maintain normovolaemia – prevention of secondary brain injury

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