ACUTE MEDICAL EMERGENCIES - PART 4 doc

Table 9.3 Haemodynamic variables in shock (adult mean values) As described before, the type of septic shock known as the toxic shock syndrome has many potential causes. However, the clinical presentation remains the same: ● temperature greater than 38·9ºC ● macular, blanching rash ● hypotension ● evidence of involvement of at least three systems. The rash can be localised or general and tends to lead to desquamation after one or two weeks in survivors. Common systems which are involved are gastrointestinal (diar- rhoea and vomiting); neurological (confusion, drowsy); renal (impaired function); muscle (myalgia, high creatine phosphokinase); hematological (leucocytosis, dissemi- nated intravascular coagulation, thrombocytopenia). Management If these patients are to survive, the source of infection needs to be removed. Repeated blood cultures are required to determine the causative organism. Antibiotic therapy should be aimed at the most likely organism. However, often a combination of a peni- cillin, aminoglycoside and metronidazole is used according to the hospital antibiotic policy. If meningococcal septicaemia is suspected give benzyl penicillin 2·4 g and ceftri- axone 1 g intravenously immediately.When there is a collection of pus, drainage will be required by either surgery or percutaneously under imaging control. The patient will require cardiovascular and respiratory support, as well as intensive monitoring of their fluid and antibiotic regimes.The former aims to maintain a high car- diac index (over 4·5 l/min/m 2 ), high oxygen delivery (above 600 ml/min/m 2 ) and tissue perfusion pressure. This usually entails intubating and ventilating the patient with sup- plemental oxygen, correction of hypovolaemia with colloid and the use of inotropes.The response to all vasoactive drugs is unpredictable. It is therefore advisable to start with a low dose and titrate further amounts until the cardiac index is sufficient to allow accept- able tissue perfusion. In adults this is usually at a level greater than 4·5 l/min/m 2 . The indications for ventilation are no different from those routinely used: ● inability to maintain an airway ● inability to maintain normal PaO 2 and PaCO 2 ● persistant tachypnoea despite adequate oxygenation and volume replacement Key points ● Maintain a high index of suspicion because diagnosing septic shock can be difficult ● Always check for the non-blanching purpuric rash of meningococcal septicaemia ● Consider the diagnosis in any ill patient with an altered conscious level and haemodynamic instability without any obvious cause Left atrial Cardiac Systemic vascular pressure output resistance (mm Hg) (l/min) (dyn/s/cm 2 ) Normal 10 5 1200 Left ventricular failure 25 2 3000 Haemorrhage 0 3 3000 Sepsis and anaphylaxis 2 12 300 THE PATIENT WITH SHOCK 131 09-AcuteMed-9-cpp 28/9/2000 4:06 pm Page 131 ● persistant metabolic acidaemia ● elevated serum lactate. Noradrenaline is frequently needed for its α agonist activity that helps counteract some of the profound vasodilatation. Neurogenic shock In the context of acute medical emergencies neurogenic shock is rare. Patients who are susceptible to spontaneous cervical vertebral subluxation include those with rheumatoid disease or Down’s syndrome. In contrast, ankylosing spondylitis can produce an inflex- ible cervical spine that fractures following minimal trauma. The effects of neurogenic shock result from the loss of sympathetic output.This gives rise to a systolic blood pressure of approximately 90 mm Hg with a heart rate of around 50 per minute. In addition the patient has warm and pink skin due to vasodilatation. However, due to an initial pressor response releasing catecholamines into the circulation, the onset of these signs can take minutes to hours to develop. This situation may persist for up to 24 hours before the levels of catecholamines fall enough to reveal the neuro- genic shock. The lack of sympathetic tone decreases the patient’s response to other types of shock. It also enhances the vagal effect produced by stimulation of the pharynx, for example, during laryngoscopy. This can lead to profound bradycardia requiring treatment with glycopyrrolate. Atropine can be used but it produces dry, thick secretions which increase the lung dysfunction. Due to the nature of the injury the patient will also present with motor and sensory loss. However, these are difficult to assess in the unconscious patient. If in doubt immo- bilise the cervical spine and request a neurosurgical/orthopaedic review. Management These patients usually require intubation as the risks of regurgitation and aspiration are increased due to the presence of a paralytic ileus, a full stomach and an incompetent gastrooesophageal sphincter. As close to 100% oxygen should be given, not least because the damaged spinal cord is very sensitive to hypoxaemia. Always maintain in-line cervi- cal spine immobilisation by an assistant holding the head or by the use of commercially available apparatus. Persistent signs or symptoms of shock must not be attributed to the presence of spinal cord injury particularly if there is evidence of haemorrage or trauma. Correction of any Key point Intubation is not contraindicated in the presence of cervical spine instability Key points ● Beware of the unconscious patient who is admitted following a fall downstairs. The initial neurological features are often attributed to an underlying stroke ● Spinal stabilisation must be maintained until specialist advice is obtained if a spinal injury is suspected from either the mechanism of the injury or the physical signs ACUTE MEDICAL EMERGENCIES: THE PRACTICAL APPROACH 132 09-AcuteMed-9-cpp 28/9/2000 4:06 pm Page 132 bleeding source is still relevant in cases of spinal injury because of the risks of hypoper- fusion of the spinal cord. In the presence of an isolated spinal cord injury, a systolic blood pressure of 80–90 mm Hg is initially acceptable and usually achieved with a fluid chal- lenge of 0·5–1 litre. Patients with an enduring bradycardia of less than 50 beats per minute should be given atropine 0·5–1 mg intravenously, and repeated if necessary until the heart rate is acceptable. If this fails, inotropes may be required but this will involve the use of invasive haemodynamic monitoring to ensure that the patient does not develop pulmonary complications due to inappropriate fluid management. Early insertion of an arterial line is necessary in these patients.This provides continu- ous, accurate blood pressure recordings as well as facilitating repeated arterial blood gas sampling. It is important that these patients are neither under- nor overtransfused. The former leads to further spinal injury, the latter leads to pulmonary oedema. As central venous pressure recording is unreliable a pulmonary artery occlusion pressure catheter should be inserted as soon as possible. The loss of vascular tone in patients with high spinal injuries causes them to be prone to postural hypotension.This can occur in tipping or lifting the patient suddenly, as well as turning the trolleys at speed. As a result there can be underperfusion of areas of the body and episodes of ventilatory–perfusion mismatch. It is therefore essential that these potential problems are prevented by the careful and coordinated movement of these patients. During the initial neurological assessment using the AVPU scale or Glasgow Coma Scale, an asymmetrical weakness may become apparent or a lack of response to periph- eral stimulation. These should be noted and a definitive neurological examination per- formed in the secondary assessment (see Chapter 7). Finally, remember to keep the patient covered by warm sheets and blankets. This not only avoids embarrassment but also prevents heat loss from vasodilatation that occurs after high spinal injuries. Following the primary assessment and resuscitation, specialist advice should be sought regarding investigations and further management. Following plain X-rays, CT scanning has become the mainstay for spinal cord injuries. Its axial slices and reconstructive capa- bilities give CT scanning the ability to visualise vertebral fractures. In addition, the degree of canal compromise can be accurately determined to within 1 mm or less. Plain CT, however, does not demonstrate the intraspinal contents other than bone fragments; for this reason contrast enhancement is required.This has been superseded by magnetic resonance (MR) scanning which is now the investigation of choice where visualisation of the contents of the spinal canal is required and for detecting ligamentous and interverte- bral disc damage. However, resuscitation equipment must be magnetic resonance imag- ing compatible. Published work has shown the advantage of giving high doses of methyl prednisolone in the first 24 hours after blunt spinal injury (see box). The reason for this improvement is not known but workers have postulated that it could be due to a decrease in lipid per- oxidation, protein degradation, catabolic activity or an increase in impulse conduction by activation of ion pumps. Following evaluation of the spinal cord injury by plain radiography, CT and MR scanning, a decision as to the need for surgical stabilisation can be more accurately The early use of methyl prednisolone following blunt spinal injury ● 30 mg/kg IV over 15 minutes immediately ● Then 5·4 mg/kg/hour for 23 hours THE PATIENT WITH SHOCK 133 09-AcuteMed-9-cpp 28/9/2000 4:06 pm Page 133 made. In the early hours of management following cervical spine injury, sufficient pro- tection to the nervous system can be afforded by inline immobilisation and log-rolling with the patient’s neck fixed in a hard collar.With radiological control, skull traction can be applied using increasing weights as necessary to maintain alignment without over- distraction. MONITORING AND ON-GOING CARE The shocked patient’s vital signs should be continuously monitored. In the shocked patient coexistent pathology can be present and for those with ischaemic heart disease, the increase in cardiac work and oxygen demand may be criti- cal. Therefore the need for high inspired levels of oxygen and accurate monitoring is extremely important. An arterial blood sample must also be sent and the result analysed. Acidosis should be initially treated with increased ventilation and fluid administration. Sodium bicarbonate is reserved for cases where the pH is less than 7.1. Accurate measurement of urinary volume will obviously require the insertion of a uri- nary catheter. This should be connected to a system permitting accurate volume mea- surement that can be recorded whenever the other vital signs are measured. In cases of hypovolaemia, hypotension indicates that at least 30% of the intravascular volume has been lost, therefore a blood transfusion will be required. The decision to transfuse the patient may also be made if there is a poor or transient response to the ini- tial fluid challenge (Table 9.4). Table 9.4 Response to a fluid challenge In the “responder” the vital signs will return to normal after the fluid challenge. However, such individuals may need an elective transfusion of fully crossmatched blood. In contrast, transiently normal vital signs that deteriorate suggest continued haemor- rhage and the need for more fluid. Ideally this should be typed blood and therefore only checked for ABO and Rhesus compatibility. Most laboratories can provide this within 15 Type of response Reason Responder Volume loss less than 1000 ml Transient responder Volume loss greater than 1000 and less than 2000 ml Non-responder Volume loss greater than 2000 ml Consider another cause for shock Monitored vital signs in hypovolaemic patients ● Respiratory rate ● Peripheral oxygen saturation ● Heart rate ● Blood pressure ● Pulse pressure ● Capillary refill ● Chest leads (ECG rhythm and wave form) ● Temperature (core and peripheral) ● Urinary output ● Glasgow Coma Scale ACUTE MEDICAL EMERGENCIES: THE PRACTICAL APPROACH 134 09-AcuteMed-9-cpp 28/9/2000 4:06 pm Page 134 minutes. If there is no recordable blood pressure uncross matched blood (O negative) is required urgently due to the loss of over 40% of the intravascular volume. Once the uncross matched blood has been given, the typed blood should be available. Coagulation abnormalities can occur after massive blood loss because of: ● dilution of clotting factors by administered fluids ● release of tissue factors which inhibit clotting ● low concentration of clotting factors in stored blood. Treatment of any type of coagulation disorder has to be guided by the results of the clotting studies and liaison with the haematologist. Do not treat any bleeding problem blindly with platelets, fresh frozen plasma and vitamin K . LATE DEVELOPMENT OF SHOCK Shock should be identified and dealt with during the primary assessment. However, it can develop, or recur, at any stage in the patient’s care. Consequently you must remain vigilant and continue to monitor and assess the patient. Should shock develop you need to repeat the primary assessment and manage the patient in the manner described ear- lier. However, you will usually be helped in this situation because there will be more information available regarding the patient’s medical history. Consequently likely causes can be checked for first. SUMMARY There are many causes of shock but all lead to inadequate delivery, or utilisation, of oxygen and glucose by vital tissues. This chapter has concentrated on the oxygenation issues. In these cases the management goal is to treat hypoxaemia and hypovolaemia whilst excluding the immediately life threatening conditions. It is also important to realise that resuscitation, though crucial, only plays a preliminary part in the patient’s long term management. It is therefore best that shocked patients receive multi-specialty input from the beginning. TIME OUT 9.3 Take a moment to write down how you would manage a 60 year old man who pre- sents after a haematemesis. Initial vital signs recorded by the nurse are: Respiratory rate 28/minute SaO 2 92% (air) Pulse rate 120/minute Blood pressure 90/60 Pale, sweating and anxious. THE PATIENT WITH SHOCK 135 09-AcuteMed-9-cpp 28/9/2000 4:06 pm Page 135 This Page Intentionally Left Blank CHAPTER 10 The patient with chest pain OBJECTIVES After reading this chapter you will be able to: ● resuscitate a patient with chest pain ● identify and instigate emergency treatment for the immediate life threatening causes of chest pain ● formulate a differential diagnosis for non immediately life threatening causes of chest pain ● discuss the investigation and management of the other causes of chest pain. INTRODUCTION Chest pain has many underlying causes and these range from the life threatening to the trivial. The nature of the pain (site, severity, radiation, and associations) varies with the actual cause, but in clinical practice immediately life threatening causes (next box) can be difficult to identify rapidly.Therefore a structured approach to care is advocated start- ing with a primary assessment and resuscitation followed by secondary assessment and emergency treatments. PRIMARY ASSESSMENT AND RESUSCITATION This concentrates on the evaluation and maintainance of the ABCs. If the patient is con- scious it is usually also possible to gain key information about their chest pain at the same time. Life threatening causes of chest pain ● Myocardial infarction ● Pulmonary emboli ● Tension pneumothorax ● Dissecting thoracic aneurysm 137 Reading: 20 minutes 10-AcuteMed-10-cpp 28/9/2000 4:15 pm Page 137 Airway Airway patency must be assessed and secured where necessary. If the patient’s conscious level is fluctuating then simple airway adjuncts may be needed. If the airway cannot be maintained despite these measures then either endotracheal intubation or surgical airway management may be needed. Breathing All patients will require high flow oxygen at 12–15 litres per minute via a non- rebreathing mask with reservoir. The rate, symmetry, and effort of respiration should be noted. Palpation in the sternal notch will determine whether there is either tracheal deviation or tug. After percussing the anterior chest wall for areas of hyperresonance or dullness, breath sounds should be auscultated and any additional sounds, such as a pleural rub, identified. Inadequate breathing should be supported – initially by bag–valve – mask ventilation and then by intubation and mechanical ventilation. Pulmonary emboli producing pleu- ritic chest pain are, in themselves, rarely life threatening. However, such a symptom should raise the clinician’s suspicion of a potential, larger embolus that may have a sig- nificant haemodynamic effect including pulseless electrical activity (PEA, or previously electromechanical dissociation (EMD)). Tension pneumothoraces are a rare cause of chest pain but are rapidly fatal if ignored. The clinician must be alert to this problem, in particular in patients with preexisting lung disease. Once the diagnosis has been made, time should not be wasted getting X-rays. An immediate needle thoracocentesis is required. This converts the tension into a simple pneumothorax and allows time for chest drain insertion. Circulation The clinician must check for the presence of an arterial pulse and assess the rate. The carotid artery is first choice but radial, carotid, and femoral arteries should be palpated to determine their pressure, volume, and radio-carotid or radio-femoral delay. Check the precordium for the position and character of the apex beat plus any thrills or heaves. Listen for the presence of normal, altered, and added heart sounds, as well as murmurs. Ideally, all patients should have IV access – the antecubital fossa is usually the easiest site. A central line may be used provided that the clinician has appropriate experience. Monitoring should include SpO 2 , pulse, blood pressure, and ECG. Immediate investigations Once access has been secured, blood should be taken for full blood count, cardiac enzymes, electrolytes, and blood glucose. If a dissecting aneurysm is suspected, blood transfusion will be required and therefore a sample should be taken for cross match. Arterial blood gas measurement is also ideally required to exclude any underlying acid–base disturbance, ventilation–perfusion mismatch and inadequate ventilation. All patients with non-traumatic chest pain will require an early 12 lead ECG as it can help in differentiating the causes of chest pain (next box). Key point A normal ECG does not exclude a myocardial infarct ACUTE MEDICAL EMERGENCIES: THE PRACTICAL APPROACH 138 10-AcuteMed-10-cpp 28/9/2000 4:15 pm Page 138 A diagnosis made on ECG should lead to rapid emergency treatment. A 12 lead ECG may be normal during the evolution of myocardial infarct. If pericarditis is present then the classic concave ST elevation occurs in the leads that lie over the affected area. SECONDARY ASSESSMENT Immediately life threatening conditions are rare, but it is important that they have been excluded or treated. Attention can then be directed to the secondary assessment where the crucial exclusions are myocardial infarction, pulmonary embolus, pneumonia, and pneumothorax.These latter two conditions are easily diagnosed radiologically; therefore, the essential management plan is to rule out myocardial infarction (ROMI) and pul- monary embolus (ROPE). Other, minor conditions can be investigated often as an out- patient. History Clinical diagnoses are frequently made on the basis of a medical history.The features of a chest pain should be, as usual, assessed in a regular and orderly sequence paying par- ticular attention to the site, character, radiation, precipitation, and relieving factors as well as any other associated symptoms. A pertinent history can provide invaluable clues as to the differential diagnosis of con- ditions giving rise to chest pain. Acute myocardial infarction patients with ECG changes should have been spotted straight away and treated appropriately.Those patients who remain will range from those with unstable angina to those with musculoskeletal pain. While the particular diagnosis in individual patients may take some time to establish, the risks of either myocardial infarction or of later complications can be rapidly assessed by further consideration of the ECG, by taking a focused history and by carrying out a brief examination. This will allow appropriate decisions about further care to be made. ECG features of immediately life threatening causes of chest pain Myocardial infarction Normal (ACEP) 1 mm (0·1 mV) ST elevation in two of the inferior leads 1 mm (0·1 mV) ST elevation in leads 1 and aVL 2 mm (0·2 mV) ST elevation in two contiguous leads New bundle branch block True posterior infarct Pulmonary emboli Normal Sinus tachycardia Atrial fibrillation Right axis deviation P pulmonale Right ventricular strain Right bundle branch block Thoracic aorta dissection Normal Signs of left ventricular hypertrophy and strain due to hypertension Acute ischaemic changes when coronary ostia are involved (rare) Heart block if the haematoma extends into the atrioventricular node (very rare) THE PATIENT WITH CHEST PAIN 139 10-AcuteMed-10-cpp 28/9/2000 4:15 pm Page 139 The ECG findings are considered first – ischaemic changes not known to be old pre- dict both a high risk of myocardial infarction and also a high risk of complications. If the ECG is normal then clinical risk factors are sought – these include any history consistent with unstable ischaemic heart disease (worsening of previously stable angina, new onset of post infarction or post coronary revascularisation angina, or pain the same as a previ- ous myocardial infarction) and findings of either hypotension (systolic blood pressure less than 120 mm Hg) or significant heart failure (crepitations not just including the bases). If more than two are present then the patient is at high risk. If one risk factor is present or there are none at all then the history should be reconsidered to see whether one of two particular scenarios that go along with a moderate risk of myocardial infarc- tion is present. These are shown below. The whole approach to clinical risk assessment is shown in Figure 10.1. This assess- ment tool is derived from the multicentre chest pain study and provides an objective, evi- dence based tool. It ensures that acute myocardial infarction patients are identified rapidly and provides a framework for subsequent care of all those remaining. Figure 10.1 Clinical risk assessment in patients with chest pain Tension pneumothorax can present with progressive dyspnoea, occasionally pleuritic pain, and in extreme cases, a cardiorespiratory arrest (see later). A similar range of presentations may be encountered in patients with pulmonary emboli. It is therefore important to enquire about the history of breathlessness and haemoptysis, as this may help in establishing the correct diagnosis. The pain from a dissecting thoracic aortic aneurysm usually starts in the centre of the chest and radiates through between the scapulae and may involve the upper limbs. It is often described as tearing but the nature of the pain may change as the dissection pro- gresses. With most of these conditions, there are no identifiable precipitating causes. ≤1 ≥2 N Y N new ischaemia acute MI Significant history Risk factors ECG changes Moderate Low High Definite AMI Scenario 1: Typical cardiac pain in a patient over 40 years old where the pain is not reproduced by palpation, is not stabbing in nature and does not radiate atypically. Scenario 2: A history of anginal pain lasting longer than one hour that was either worse than usual angina pain or as bad as the pain of a previous acute myocardial infarction. ACUTE MEDICAL EMERGENCIES: THE PRACTICAL APPROACH 140 10-AcuteMed-10-cpp 28/9/2000 4:15 pm Page 140 [...]... clinical features are shown in the box Non-neurological features associated with cerebral malaria Anaemia Spontaneous bleeding from the gastrointestinal tract Jaundice Hypoglycaemia Shock Oliguria Acute renal failure Pulmonary oedema 165 ACUTE MEDICAL EMERGENCIES: THE PRACTICAL APPROACH Diagnosis Malaria should be considered in the differential diagnosis of any acute febrile illness until it can be excluded... reaction to light Check for meningeal irritation – if there are no contra-indications Remember, at this stage, you are looking for conditions which are immediately life threatening! Consider: ● ● ● ● ● Hypoglyceamia Antedotes e.g naloxone if pinpoint pupils/needle track marks Antibiotics Acyclevir Antiepileptic drugs 149 ACUTE MEDICAL EMERGENCIES: THE PRACTICAL APPROACH E – exposure The patient must be... combination fails to relieve pain, then opiates 143 ACUTE MEDICAL EMERGENCIES: THE PRACTICAL APPROACH should be used Irrespective of the patient’s age, thrombolysis must be started as soon as possible provided there are no contraindications (next box) Clinical trials have shown that the beneficial effect of thrombolysis is significantly reduced with time, particularly if it is started over 12 hours after... thalamus to synapse in the cortex There is no specific individual area in the cortex that is responsible for the conscious state, but the coordinated interaction of many cortical areas is required 147 ACUTE MEDICAL EMERGENCIES: THE PRACTICAL APPROACH Cerebral metabolism Glucose and oxygen are the essential fuels for cerebral metabolism The brain only has a small store of glucose This supply is maintained... pericarditis Sharp Left arm >> right arm Very rare – throat Deep inspiration Coughing Postural variation (depending on site of inflammation) Postural variation Occasionally pleuritic Pericardial rub 141 ACUTE MEDICAL EMERGENCIES: THE PRACTICAL APPROACH Table 10.2 Clinical features of chest pain caused by respiratory disease Pleuritic Site Character Radiation Precipitation Relief Associated symptoms Clinical... Complications of meningitis Raised intracranial pressure Seizures Hyponatraemia Venous sinus thrombosis Cranial nerve deficit Hydrocephalus 161 ACUTE MEDICAL EMERGENCIES: THE PRACTICAL APPROACH Tuberculous meningitis There has been an increased incidence of tuberculosis in many parts of the world, related to the human immunodeficiency viral infection These patients have a high risk of meningeal involvement Other... A normal endoscopy, however, does not exclude this disease and formal pH, manometry and a semisolid phase barium swallow may be required to confirm the diagnosis – similarly for diffuse spasm 145 ACUTE MEDICAL EMERGENCIES: THE PRACTICAL APPROACH DIAGNOSTIC PITFALLS ● Patients with chest pain, irrespective of the cause, will manifest clinical features of anxiety ● Always reassess every episode of chest... myocardial infarction will be transferred to coronary care, whilst patients with other causes of chest pain will be managed on a medical ward Appropriate investigations will then be required to confirm or refute these conclusions The choice will depend upon which body system(s) is involved 144 THE PATIENT WITH CHEST PAIN INVESTIGATIONS ECG All patients with chest pain should have continuous electrocardiograph... infarction and is often used to identify potential candidates for coronary angiography In addition, it is particularly useful in detecting ischaemic chest pain when the exercise provokes chest pain identical to that experienced by the patient in association with ST depression Chest X-ray A chest X-ray is of limited diagnostic use in patients with angina and myocardial infarction unless the latter is... Response Spontaneous To speech To painful stimuli Nil 150 Score 4 3 2 1 THE PATIENT WITH ALTERED CONSCIOUS LEVEL Verbal response Response Orientated Confused Inappropriate words Incomprehensible sounds Nil Score 5 4 3 2 1 If assessment of a verbal response is not possible, for example, due to an in situ endotracheal tube, then this fact should be documented in the patient’s notes Motor response Response . of a previous acute myocardial infarction. ACUTE MEDICAL EMERGENCIES: THE PRACTICAL APPROACH 140 10-AcuteMed-10-cpp 28/9/2000 4: 15 pm Page 140 Risk factors need to be sought, in particular a family. percussion note emphysema Reduced breath sounds ACUTE MEDICAL EMERGENCIES: THE PRACTICAL APPROACH 142 10-AcuteMed-10-cpp 28/9/2000 4: 15 pm Page 142 Table 10 .4 Clinical features of chest wall pain Table. peripheral) ● Urinary output ● Glasgow Coma Scale ACUTE MEDICAL EMERGENCIES: THE PRACTICAL APPROACH 1 34 09-AcuteMed-9-cpp 28/9/2000 4: 06 pm Page 1 34 minutes. If there is no recordable blood pressure