ITU

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12 ITU

Shock

Case history (1)

A 60-year-old bank manager presents with crushing central chest pain. This started 45 minutes ago and has remained constant ever since.

On examination he is pale and clammy. His pulse is 100/min, poor volume and BP 90/60.

Diagnosis.

Shock – cardiogenic; ECG shows evidence of anterior myocardial infarction.

Case history (2)

A 50-year-old man who works in a bar has been brought to hospital vomiting a large amount of blood. He gave no history of upper abdominal pain but did admit to drinking a bottle of whiskey a day and occasional beers as well.

He also admits to a previous hospital admission with abdominal swelling which was due to alcoholic liver disease. He was told that his liver disease was bad and that he must stop drinking and take propranolol regularly as he had varices on endoscopy. He had not stopped drinking, nor was he taking his propranolol.

On examination he is sweating profusely with visible shaking of his extremeties. His pulse rate is 120/min with a blood pressure of 90/60.

Diagnosis.

Shock – hypovolaemia due to blood loss, probably from oesophageal varices.

Remember

• Shock is a life-threatening condition in which the patient is suffering global hypoxic injury

• Establish clear airway

• Oxygen must be given immediately to all haemodynamically unstable patients.

Physiology (Fig. 12.1)

Shock is ‘inadequate tissue oxygenation’ where there is failure of the circulatory system due to:

• Failure of the heart to maintain an adequate cardiac output, e.g. myocardial infarction

• Reduction in the volume of blood within the circulation, e.g. haemorrhage

• Loss of vascular tone within the circulatory system, e.g. septicaemia

• Obstruction to the circulation, e.g. pulmonary embolism.

Figure 12.1 The sympatho-adrenal response to shock showing the effect of increased catecholamines on the left of the diagram and the release of angiotensin and aldosterone on the right. Both mechanisms result in maintaining the blood pressure and cardiac output in shock.

Causes of shock

• Cardiogenic: myocardial infarction, tamponade, aortic dissection, pulmonary embolism

• Sepsis: infective causes, e.g. pneumonia, urinary tract infection or meningococcal septicaemia or ‘systemic inflammation’, resulting from trauma, post-surgery or anaphylaxis

• Hypovolaemia: profound dehydration, haemorrhage.

Remember

A patient might have more than one cause of shock, e.g. Case 2 may have an alcoholic cardiomyopathy (pump failure) as well as his haematemesis (decreased blood volume).

Is the shock state in Case 1 due to myocardial infarction, an obstructed circulation or other shock-inducing factors?

A history in a shocked patient of chest pain associated with ECG evidence of a myocardial infarction makes the diagnosis in this case. However, be careful because ECG changes with tachyarrhythmias and some ST segment changes which look characteristic of myocardial ischaemia can also occur in other types of shock.

Is the shock state in Case 2 due to fluid loss? If so, what fluid and from where?

In this case the blood loss is obvious, i.e. haematemesis. Try and estimate from the patient how much was lost. In other cases blood loss might be concealed, e.g. pancreatitis.

Clinical examination

In assessing the shocked patient the following indices should be monitored:

• Pulse rate and respiratory rate

• Peripheral venous filling/capillary filling

• Limb temperature

• Arterial blood pressure

• Urinary output

• Mental status.

Investigations

• Haemoglobin and haematocrit, U&Es, LFTs, troponin estimation

• ECG and monitor

• Central venous pressure (see p. 225)

• If the CVP is low (< 5 mmHg) fluid replacement is necessary

• If 10 mmHg or more, fluid replacement is probably not required immediately

Case 1 – has a problem with the circulatory pump and probably needs no extra intravascular fluid administration.

Case 2 – the haematemesis patient – has lost circulating volume with a low central venous pressure. His problems are with the plumbing circuit not the heart pump but his condition might be compounded by coagulation and biochemical disturbances consequent upon hepatic insufficiency.

Other investigations (see Fig 12.2)

• Arterial blood gas analysis: in hypovolaemic shock (as in all shock states) there is a metabolic acidosis with a high hydrogen ion concentration and low bicarbonate concentration. In cases with respiratory complications the pO₂ and pCO₂ values will help indicate the need for ventilatory support.

• Lactate levels: blood lactate levels rise approximately in proportion to the severity of the shock.

• X-rays: these are usually of little value in the acute stages of shock management. A CXR will exclude any treatable pathology, such as a pneumothorax or haemothorax often complicating insertion of monitoring lines. A CT scan may be helpful in, for example, a case of trauma.

Figure 12.2 Management of shock. Patients require intensive nursing care.

How would you treat?

Both patients should be admitted to high-dependency nursing units in the first instance as their MEWS scores were > 5.

Case 1

In cardiogenic hypotension key issues are pain relief, arrhythmia management and treatment of pulmonary oedema. Pain relief by incremental doses of intravenous opiates will aid reduction in myocardial oxygen consumption. Correcting electrolyte disturbances, hypoxia and controlling angina pain might assist in arrhythmia management. Temporary transvenous pacing might be required for significant bradycardia. Continuous infusion of vasodilators (e.g. glyceryl trinitrate 10–200 µg/min) plus diuretics (e.g. furosemide 40 mg) is needed for pulmonary oedema. Acute revascularisation (thrombolysis, angioplasty) might also be indicated. In the context of persistent hypotension, infusion of inotropic agents such as dobutamine (e.g. 2.5–10 µg/kg/min) might be necessary whilst correctable abnormalities are sought (e.g. acute mitral regurgitation following papillary muscle rupture or the development of an ischaemic ventricular septal defect). Percutaneous insertion of an intra-aortic balloon counterpulsation pump may be necessary for refractory cardiogenic hypotension following transfer to a specialist centre as a prelude to surgical intervention.

Progress.

This man initially improved on ionotropes, diuretics and vasodilatory therapy. However, he remained hypotensive, BP < 90 with poor output. He was transferred to the Cardiac Centre for insertion of an intra-aortic balloon pump. He did not respond and died 3 days later (mortality is 79% for cardiogenic shock).

Case 2

In hypovolaemic hypotension the principal issues are the reduction in further fluid loss and simultaneously restoring fluid volumes via wide-bore intravenous cannulae. Infusion of red cells provides sufficient oxygen transport capacity (a target of 7–9 g/dL is broadly accepted). Fresh frozen plasma (e.g. to obtain a target INR of < 1.5) might be necessary. At the earliest opportunity the patient with haematemesis will require endoscopy to find the bleeding lesion and treat (see p. 67).

Progress.

This man was successfully resuscitated and variceal banding was performed at endoscopy. He left hospital after 7 days and was referred to the local Liver Unit for consideration of liver transplantation (Child’s Grade C alcoholic liver disease). He did not attend the clinic and was readmitted 6 weeks later in hepatic coma and died.

Case history (3)

A 68-year-old man is brought to A&E by ambulance. His wife says that he developed abdominal pain 4 days ago which has got progressively worse. He has always suffered from indigestion and pain in the stomach area after food, for which he has taken antacids with some relief.

On this occasion the pains got worse and she said her husband had refused to get out of bed and appeared to be confused and disorientated. She had called an ambulance, which brought him to hospital.

On examination he was pyrexial at 39°C. He was pale and unsure of his surroundings and moaning about his abdominal pain. His pulse was 120 beats/min with a blood pressure of 90/40 and he had a cold nose. He was breathless and his O₂ sats were 90%.

Abdominal examination revealed a distended abdomen, tender to touch, with absent bowel sounds.

What is the cause of shock in this patient?

The patient has septic shock, probably secondary to intra-abdominal sepsis. He will need fluid resuscitation and urgent investigations and probably a laparotomy.

How would you manage this case? (see Fig. 12.2)

Immediate action

• Correct hypoxaemia: high-flow O₂ via a face mask.

• Determine cause: examination, chest and abdominal X-ray, ECG, ABGs, FBC, U&Es, amylase, blood cultures.

• Initiate treatment: IV fluid resuscitation with 0.9% saline, inotropes if no response to fluid resuscitation.

• Insert a urinary catheter and monitor urinary output.

Shock is a medical emergency. The longer it persists, the lower the chance of recovery because secondary injury, from coexistent hypoxaemia and delayed reperfusion, is now recognised to cause further cytokine activation and the development of multiple organ failure (MOF).

Information

The medical records of many patients admitted to the ICU from the ward show progressive evidence of impending collapse – increasing heart rate, oliguria, tachypnoea or confusion.

Act before shock has become established!

Pathophysiology of septic shock

In sepsis, hypotension primarily results from impaired vascular tone. Sympathetic activation often leads to a high cardiac output with a low systemic vascular resistance. Hypovolaemia can occur from interstitial fluid losses due to widespread endothelial dysfunction and reduced venous tone. In more profound sepsis, myocardial depression also occurs due to circulating cytokines such as tumour necrosis factor (TNF).

Summary

Timely intervention in patients with sepsis might prevent the progression of shock. Fluid resuscitation and treatment aimed at the primary cause should be instituted rapidly and high-flow oxygen given to limit regional hypoxaemia. Prognosis is dependent on cause and response to treatment. For instance, mortality from urinary sepsis has a better prognosis than a similar clinical situation resulting from peritonitis.

Progress.

This man had peritonitis secondary to a perforated ulcer. He was resuscitated and admitted to the ITU. He later had a laparotomy (a laparoscopic surgeon was unavailable) with washout of the peritoneum and oversewing of the ulcer, with an omental patch. He remained in ITU, needing inotropic support and ventilation for 4 days and was then transferred to the ward. He eventually made a good recovery. Helicobacter pylori eradication was given.

Acute lung injury/Acute Respiratory Distress Syndrome (ARDS)

Case history

You are called urgently to the emergency department when on take. A 35-year-old known drug user has been sent urgently to the hospital having been found unconscious. The Glasgow Coma Score (GCS) is 5, BP 100/60 with a respiratory rate of 20 and SaO₂ on high-flow O₂ therapy is 85%.

What are the possible causes of depressed consciousness and what are your immediate actions?

• You need to consider intoxication, hypoglycaemia, respiratory failure, head injury or a post-ictal state.

On examination, look for evidence of focal neurological signs, pinpoint pupils, trauma to the head or evidence of seizures such as tongue laceration, incontinence.

• Ensure airway not obstructed, establish IV access, take blood gases, blood glucose and blood and urine for toxicology.

• ABG analysis reveals pH 7.2, PaO₂ 6.4, PaCO₂ 2.5, lactate 4.1 mmol/L.

What do these results indicate?

• Acute type 1 respiratory failure with a metabolic (lactic) acidosis.

• There is vomitus around the mouth and on his clothing. The chest X-ray shows patchy shadowing at the right base.

• Following naloxone administration he becomes agitated, moving all limbs, but does not respond purposely to command.

What is the immediate management?

Respiratory failure is probably related to aspiration of vomitus. Intubation and IPPV are indicated. CPAP or non-invasive ventilation are contraindicated because of danger of further vomiting and lack of cooperation.

He was transferred to the ICU. On the post-take ward round next morning, ventilatory pressures are high for standard tidal volumes and he remains hypoxic on F_iO₂ 100%. Your consultant suggests you make a short presentation on acute respiratory distress syndrome (ARDS) to the students at the lunch-time meeting.

Key features of acute lung injury/ARDS

See Figure 12.3:

• Pulmonary infiltrates: due to an increase in lung interstitial fluid not related to heart failure; by definition pulmonary artery occlusion pressure < 18 mmHg.

• A reduction in pulmonary compliance: i.e. stiff lungs, resulting in high inflation pressures.

• Profound gas exchange abnormalities defined as PaO₂ : F_iO₂ ratio < 300 mmHg for acute lung injury (ALI) or < 200 mmHg for ARDS.

Figure 12.3 Chest radiograph appearances in adult respiratory distress syndrome (ARDS). Bilateral diffuse alveolar shadowing with air bronchograms and no cardiac enlargement.

From Kumar and Clark Clinical Medicine 8th edn, 2012.

Causes

• Severe sepsis, e.g. peritonitis, septicaemia

• Pulmonary aspiration (as in this case)

• Multiple trauma and massive transfusion

• Post-cardiac bypass syndrome

• Pancreatitis

• Toxic fume exposure including smoke inhalation

• Cerebral injury, e.g. subarachnoid haemorrhage.

Pathophysiology

Profound hypoxaemia results from venous admixture or shunting of deoxygenated blood through poorly or unventilated lung units. This arises because:

• Endothelial dysfunction leads to widespread interstitial oedema and impaired alveolar capillary perfusion.

• The stiff (low-compliance) lungs result in reduced tidal volume and reduced end expiratory lung volume – this then causes small airway collapse. Once collapsed, Laplace’s law explains why it is difficult to re-expand the airway (consider the difficulty in initially blowing up a balloon).

• Additional small airway pathology, particularly with direct lung injury, e.g. smoke inhalation.

• The lung can be likened to a wet sponge – the dependent sponge is waterlogged and the air spaces collapsed. Only the non-dependent areas of the lung might be contributing to gas exchange. The additional component of airway inflammation in some causes of ARDS explains the high mortality associated with direct lung injury (> 60%).

Management

The high mortality of ARDS is critically dependent on resolution of the primary cause. Treatment of the lung is essentially supportive. Avoidance of further injury by tolerating relative hypoxaemia (aiming to limit oxygen toxicity by F_iO₂ < 70%) and allowing permissive hypercapnia (limiting tidal volume to avoid barotrauma – overdistension of functioning lung and risk of pneumothorax). Ventilatory techniques include:

• Deep sedation and neuromuscular paralysis to increase chest wall compliance. A semi-recumbent bed position unless contraindicated.

• Small tidal volumes (6 mL/kg of predicted body weight) and prolonged inspiratory time to limit airway pressure.

• Use of a minimum amount of PEEP (positive end-expiratory pressure) to recruit lung units.

• Prone positioning to improve {Vdot}/{Qdot} matching and clearance of lung secretions.

Experimental methods include:

• Inhaled nitric oxide to overcome hypoxic pulmonary vasoconstriction and improve {Vdot}/{Qdot} matching and reduce pulmonary hypertension.

• Rescue therapy with steroids to limit the proliferative fibrotic process of lung repair.

• High-frequency ventilation.

• Extra corporeal membrane oxygenation.

Outlook

Mortality from ALI/ARDS remains high (overall 30–40%). Lung remodelling might, however, result in considerable eventual recovery. Progress of the underlying disease, hospital-acquired infection or the development of cardiogenic shock secondary to right ventricular failure are critical in determining survival.

Progress.

The patient developed multi-organ failure with impaired hepatic synthesis including coagulopathy, cholestatic jaundice and acute tubular necrosis requiring haemofiltration. Antibiotic therapy initially was IV cefuroxime infusion 1.5 g 6-hourly and metronidazole 500 mg IV 8-hourly, but subsequently Pseudomonas was cultured from respiratory secretions and IV piperacillin was started. A week later a tracheostomy was performed and ventilatory support was progressively weaned over the next 3 weeks. He was discharged from hospital 6 weeks after admission.

Further reading

Herridge MS, Tansey CM, Matte A, et al. Functional disability 5 years after acute respiratory distress syndrome. N Engl J Med. 2011;364:1293–1304.

Patekh D, Dancer RC, Thickett DR. Acute lung injury. Clin Med. 2011;11:615–618.

Wheeler AP, Bernard GR. Acute lung injury and the acute respiratory distress syndrome. Lancet. 2007;369:1556–1565.

Related

Kumar & Clarks Cases in Clinical Medicine