Intensive care medicine

Intensive care medicine (or ‘critical care medicine') is concerned mainly with the management of patients with acute life-threatening conditions (‘the criti-cally ill') in a specialized unit. It also encompasses the resuscitation and transport of those who become acutely ill, or are injured, either elsewhere in the hospital or in the community. An intensive care unit (ICU) has the facilities and expertise to provide cardiorespiratory support to these sick patients, some of whom also have kidney or liver failure, and management of this is described in the relevant chapters.

All patients admitted to the ICU require skilled nursing care (patient to nurse ratio of 1 : 1) and physiotherapy. Many require nutritional support and the enteral route should be used where possible (p. 124). General medical management includes management of pain and distress with analgesics and sedation as necessary, the prevention of venous thrombosis, pressure sores and constipation, and insulin infusions to normalize blood sugar. H2-receptor antagonists are indicated in certain high-risk individuals to prevent stress-induced peptic ulceration. A number of scoring systems, such as the Acute Physiology and Chronic Health Evaluation (APACHE) score, are in use to evaluate the severity of the patient's illness and progress.

High dependency units (HDUs) offer a level of care intermediate between that available on the general ward and that provided in an ICU. They provide monitoring and support for patients with acute (or acute on chronic) single organ failure and for those who are at risk of developing organ failure, includ-ing facilities for short-term ventilatory support and immediate resuscitation. They can also provide a ‘step-down' facility for patients being discharged from intensive care.

Patient selection - withholding and withdrawing treatment

It is essential that only those patients who are likely to benefit from intensive care are admitted to the unit. For some critically ill patients admission to ITU is inappropriate because prognosis is clearly hopeless and admission to ITU

will simply prolong the process of dying, prolong their suffering and that of their relatives and take up limited resources without benefit. A decision not to admit a patient to ITU is based on their previous health and quality of life, the primary diagnosis and the prognosis of the underlying condition. These decisions should be made in conjunction with the medical and nursing staff, the patient and relatives and documented in the medical records.

Critical care outreach and early warning systems

Within an acute hospital there are patients on general wards who are ‘at risk' and deteriorating who may require care above the ‘general level'. Prompt recognition of these patients and institution of expert treatment will often prevent their progression to severe illness. Critical care outreach is an organ-izational approach to ensure high-quality care for these patients. Outreach services have three aims:

■ Avert admissions to ITU or ensure that admissions are timely, by early identification of patients who are deteriorating

■ Enable discharges from ITU by supporting the continued recovery of discharged patients, and their relatives, on wards and after discharge from hospital

■ To share critical care skills with staff on the ward and in the community.

Terminal cardiovascular, neurological or respiratory collapse is often pre-ceded by a period of abnormal basic physiological observations during which time potential life-saving therapeutic interventions may be initiated. The Modified Early Warning Score (MEWS, Table 12.1) is a cumulative score based on routine ward observations which acts as a ‘tracker' to ‘flag up' patients who should be given immediate priority. Hospital protocols vary but in general a MEWS score of 4 or more indicates the need for urgent medical review and assessment and this will in some cases result in ITU admission.

ACUTE DISTURBANCES OF HAEMODYNAMIC FUNCTION (SHOCK)

The term ‘shock' is used to describe acute circulatory failure with inadequate or inappropriately distributed tissue perfusion resulting in decreased oxygen delivery to the tissues. The effects of inadequate tissue perfusion are initially reversible but prolonged oxygen deprivation leads to critical derangement of cell processes and eventually cell necrosis, end-organ failure and death. Thus the prompt recognition and treatment of shock is essential. The causes of shock are listed in Table 12.2. Shock is often the result of a combination of these factors, e.g. in sepsis distributive shock is frequently complicated by hypovolaemia and myocardial depression.

Table 12.2 Causes of shock
Hypovolaemic (reduced preload)
Haemorrhage: trauma, gastrointestinal bleeding, fractures, ruptured aortic aneurysm
Fluid loss: burns, severe diarrhoea, intestinal obstruction (fluid accumulates in the intestine)
Cardiogenic (pump failure)
Myocardial infarction
Myocarditis
Atrial and ventricular arrhythmias
Bradycardias
Rupture of a valve cusp
Obstructive
Obstruction to outflow: massive pulmonary embolism, tension pneumothorax
Restricted cardiac filling: cardiac tamponade, constrictive pericarditis
Distributive (decrease in systemic vascular resistance)
Vascular dilatation: drugs, sepsis
Arteriovenous shunting
Maldistribution of flow, e.g. sepsis, anaphylaxis

Pathophysiology

Sympathoadrenal In response to hypotension there is a reflex increase in sympathetic nervous activity and catecholamine release from the adrenal medulla. The resulting vasoconstriction, increased myocardial contractility and heart rate help restore blood pressure and cardiac output. Activation of the renin-angiotensin system also leads to vasoconstriction and salt and water retention, which help to restore circulating volume.

Neuroendocrine response

There is release of the pituitary hormones: ACTH, vasopressin and endogenous opioids. Cortisol release causes fluid retention and antagonizes insulin. However, the cortisol response to ACTH is blunted in septic shock but the clinical significance of this is not known. There is release of glucagon which, together with catecholamines, raises blood sugar.

Release of mediators Severe infection, the presence of large areas of damaged tissue (e.g. following trauma or extensive surgery) or prolonged/ repeated episodes of hypoperfusion can trigger a massive inflammatory response with activation of leucocytes, complement and the coagulation cascade. This is beneficial when targeted against local areas of infection or necrotic tissue but dissemination of this response can produce shock and widespread tissue damage.

■ Cell wall components from Gram-negative (lipopolysacharride) and Gram-positive (e.g. lipoteichoic acid) bacteria form a complex with specific serum proteins before attaching to a cell surface marker (CD14) and triggering a cascade of membrane bound (toll-like receptor family) and intracellular signaling pathways (MyD 88, NF-kB). This in turn leads to release of reactive oxygen and nitrogen species that kill bacteria, pro-inflammatory cytokines (tumour necrosis factor, interleukin-1 and -6) which mediate inflammation and the metabolic response, and anti-inflammatory cytokines (interleukin-10) which if excessive can cause inappropriate immune hyporesponsiveness.

■ Pro-inflammatory cytokines promote adhesion of activated leucocytes to the vessel wall and subsequent extravascular migration leading to tissue damage and organ dysfunction.

■ Platelet activating factor and lysosomal enzymes (by converting inactive kininogens to vasoactive kinins) cause increased vascular permeability.

■ Nitric oxide produced by vascular endothelial cells under the influence of certain cytokines leads to vasodilatation, hypotension and reduced reactivity to adrenergic mediators.

Microcirculatory changes In the early stages of septic shock there is vasodilatation, increased capillary permeability with interstitial oedema, and arteriovenous shunting. Vasodilatation and increased capillary permeability also occur in anaphylactic shock. In the initial stages of other forms of shock, and in the later stages of sepsis and anaphylaxis, there is capillary sequestra-tion of blood. Fluid is forced into the extravascular space, causing interstitial oedema, haemoconcentration and an increase in plasma viscosity.

Activation of the coagulation system occurs in all forms of shock, leading to platelet aggregation, widespread intravascular thrombosis and inadequate tissue perfusion, with the development of disseminated intra-vascular coagulation (DIC, see p. 235).

Progressive organ failure may develop as a result of the disseminated inflammatory response and microcirculatory changes. In multiple organ dys-function syndrome (MODS), also known as multiple organ failure (MOF) the lungs are usually affected first with the development of the acute respiratory distress syndrome (ARDS). The mortality in MODS is high and treatment is supportive.

Clinical features

The history will often indicate the cause of shock, e.g. a patient with major injuries (often internal and thus concealed) will often develop hypovolaemic shock. A patient with a history of peptic ulceration may now be bleeding into the gastrointestinal tract, and rectal examination will show melaena. Anaphy-lactic shock develops in susceptible individuals after insect stings and eating certain foods (Emergency Box 12.1).

Emergency Box 12.1
Anaphylactic shock
Pathophysiology

Massive release of mediators from mast cells and basophils induced by cross-linking of surface IgE with trigger antigen (e.g. penicillin, latex, bee sting, radiographic contrast media, eggs, peanuts, shellfish) leads to increase in vascular permeability, vasodilatation and respiratory smooth muscle contraction.
Diagnosis
Typical symptoms and signs (p. 577) developing after exposure to an agent known to provoke anaphylaxis.
Management
Remove the precipitating cause, e.g. stop administration of the offending drug
Oxygen high flow
Adrenaline 0.5 mL of a 1 : 1000 solution (500 μg) injected intramuscularly if life-threatening features (respiratory distress or shock). Repeat in 5 minutes if no clinical improvement. Intravenously (5 mL 1 : 10 000) only if cardiac arrest. Half doses of adrenaline for patients taking amitriptyline, imipramine, or β-blocker
Fluids 500–1000 mL 0.9% saline i.v.
Chlorphenamine (antihistamine) 10 mg i.m. or i.v. over 1–2 minutes
Hydrocortisone 200 mg i.m. or i.v. over 1–2 minutes
Admit patient for observation (6–8 hours) because of risk of second late reaction
Prevent further attacks. Refer to an immunologist or allergist, identify responsible allergen (careful history, skin testing, serum antibody tests by RAST or ELISA). Patients who have had an attack of anaphylaxis and who are at risk of developing another should carry a preloaded syringe of adrenaline for i.m. self-administration (e.g. Epipen device) and wear
an appropriate information bracelet (e.g. Medic Alert).

Hypovolaemic shock Increased sympathetic tone causes tachycardia (pulse > 100/min), sweating and peripheral vasoconstriction (as blood is redirected from the periphery to vital organs) leading to inadequate tissue perfusion with cold clammy skin and slow capillary refill (>3 seconds). Capillary refill is the number of seconds for the skin of the patient's digit to turn pink again after compression for 5 seconds. The blood pressure (particu-larly when supine) may be maintained initially, but later hypotension super-venes (systolic BP < 100 mmHg) with oliguria, tachypnoea, confusion and restlessness.

Cardiogenic shock Additional clinical features are those of acute heart failure, e.g. raised jugular venous pressure (JVP), pulsus alternans (alternat-ing strong and weak pulses), a ‘gallop' rhythm (additional 3rd and 4th heart sounds), basal crackles and pulmonary oedema.

Mechanical shock Muffled heart sounds, pulsus paradoxus (pulse fades on inspiration), elevated JVP and Kussmaul's sign (JVP increases on inspira-tion) occur in cardiac tamponade. In massive pulmonary embolism there are signs of right heart strain, with a raised JVP with prominent ‘a’ waves, right ventricular heave and a loud pulmonary second sound.

Anaphylactic shock Onset of symptoms is usually within 5-60 minutes of antigen exposure. Profound vasodilatation leads to warm peripheries and hypotension. Urticaria, angio-oedema, wheezing, and upper airway obstruc-tion due to laryngeal oedema may all be present.

Sepsis is an infection with evidence of a systemic inflammatory response (Table 12.3). There may be progression to severe sepsis and/or septic shock. Sepsis in elderly people or in the immunosuppressed is common without the classic clinical features of infection. The systemic inflammatory response syndrome also occurs with severe burns, trauma and acute pancreatitis and these conditions may therefore mimic infection.

Table 12.3 Differing degrees of severity of sepsis
Sepsis – systemic inflammatory response syndrome (SIRS) associated with infection
SIRS is two or more of:
Fever >38°C or hypothermia <36°C
Tachycardia: heart rate > 90 beats/min
Tachypnoea: respiratory rate > 20 breaths/min or PaCO2 < 4.3 kPa
Leucocytosis (white blood cell count >12 × 109/L), leucopenia (white cell count <4 × 109/L) or bandaemia (>10% immature forms)
Severe sepsis – sepsis with dysfunction of one or more organs:
Kidneys – creatinine > 177 μmol/L or urine output < 0.5 ml/kg/h for 2 h
Coagulation – platelets < 100, aPTT > 60 s, INR > 1.5
Respiratory – new or increased oxygen needs to keep SpO2 > 90%
Liver – bilirubin > 34 μmol/L
Tissue hypoperfusion: systolic BP < 90 mmHg, MAP > 65 mmHg, drop in > 40 mmHg from patient’s normal BP or serum lactate > 2 mmol/L
Septic shock – persisting tissue hypoperfusion after a fluid challenge:
Evidence of tissue hypoperfusion after an intravenous fluid bolus with saline 0.9% or Hartmann’s solution
MAP, mean arterial pressure over a cardiac cycle, approximated from systolic and diastolic pressures

Management

This is summarized in Emergency Box 12.2. The underlying cause must be identified and treated appropriately. Whatever the aetiology of shock, tissue blood flow and blood pressure must be restored as quickly as possible to avoid the development of multiple organ failure.

Expansion of the circulating volume (preload) Volume replacement is necessary in hypovolaemic shock and also in anaphylactic shock. Fluid is also given to patients with severe sepsis where there is vasodilatation, sequestration of blood and loss of circulating volume secondary to capillary leakage. These patients have evidence of organ dysfunction but may not

Emergency Box 12.2
Management of shock
Ensure adequate oxygenation and ventilation

• Maintain patent airway: use oropharyngeal airway or endotracheal tube if necessary
• Oxygen 15 L/min via facemask with reservoir bag unless oxygen restriction necessary (p. 521)
• Support respiratory function early: non-invasive or mechanical ventilation
• Monitor: respiratory rate, blood gases and chest X-ray
Restore cardiac output and blood pressure
• Lay patient flat or head-down
• Expand circulating volume with appropriate fluids given quickly via large-bore cannulae
• Inotropic support, vasodilators, intra-aortic balloon counterpulsation in selected cases
• Monitor in all: skin colour, pulse, blood pressure, peripheral temperature, urine output, ECG
• Monitor in selected cases: CVP monitoring, cardiac function/output
Investigations
• All cases: FBC, serum creatinine and electrolytes, blood glucose, liver
biochemistry, coagulation, blood gases, ECG
• Selected cases: culture of blood, urine, sputum, pus and CSF, blood lactate, D-dimers, echocardiogram
Treat underlying cause
• Haemorrhage, sepsis, anaphylaxis
Treat complications
• Coagulopathy, acute kidney injury, etc.

necessarily be hypotensive (Table 12.3). High filling pressures may also be needed in mechanical shock. Care must be taken to prevent volume overload, which leads to a reduction in stroke volume and a rise in left atrial pressure with a risk of pulmonary oedema. The choice of fluid depends on the clinical situation.

■ Blood is given for haemorrhage as soon as it is available. Complications of massive blood transfusion are hypothermia (minimized by using a blood warmer during infusion), coagulopathy (stored blood has almost no effective platelets and is deficient in clotting factors), hypocalcaemia (citrate anticoagulation in stored blood binds calcium), hyperkalaemia (passive leakage from stored red cells), and acute lung injury due to microaggregates in stored blood. The platelet count, prothrombin time, activated partial thromboplastin time, plasma calcium and potassium should be measured after rapid transfusion of 3-5 units of blood.

■ Crystalloid (0.9% saline or Hartmann's solution, p. 326) is given for acute blood loss before blood becomes available, and for volume replacement in anaphylactic shock and severe sepsis. There has been considerable debate of the merits of crystalloid versus colloid in volume resuscitation and in most situations there are no apparent clinical differences. In severe sepsis 500-1000 ml boluses crystalloid is given over 30 minutes with the aim of maintaining a central venous pressure 8-12 mmHg, mean arterial pressure > 65 mmHg and urine output > 0.5 ml/kg/hour.

Myocardial contractility and inotropic agents Myocardial contractility is impaired in cardiogenic shock and at a later stage in other forms of shock as a result of hypoxaemia, acidosis and the release of mediators. The treat-ment of acidosis should concentrate on correcting the cause; intravenous bicarbonate should only be administered to correct extreme (pH < 7.0) per-sistent metabolic acidosis. Drugs that impair cardiac performance, e.g. beta-blockers, should be stopped. When the signs of shock persist despite adequate volume replacement (indicated by a CVP (see below) of 8-12 mmHg), inotropic agents are administered. Inotropic agents are administered via a large central vein and the effects must be carefully monitored. The inotropic agents used and their clinical effects are shown in Table 12.4. The particular agent used depends on the values for mean arterial pressure, cardiac output and personal preference.

Additional treatment Vasodilators, e.g. sodium nitro-prusside and iso-sorbide dinitrate, may be useful in selected patients who remain vasocon-stricted and oliguric despite adequate volume replacement and a satisfactory blood pressure. Finally, in patients with a potentially reversible depression of left ventricular function (e.g. cardiogenic shock secondary to a ruptured interventricular septum), intra-aortic balloon counterpulsation (IABCP) is used as a temporary measure to maintain life until definitive surgical treatment can be carried out.

Table 12.4 Inotropic agents used in the management of shock

Inotropic agent

Sympathomimetic and dopaminergic (D) effects and main clinical use

Adrenaline

Low dose (0.06–0.1 μg/kg/min), β-adrenergic effects predominate with increase in cardiac output and fall in systemic vascular resistance (SVR). High dose (>0.18 μg/kg/min), α1-adrenergic effects predominate with increased SVR. This may increase renal perfusion pressure and urine output but excessive vasoconstriction
leads to decreased cardiac output, oliguria and peripheral gangrene
Potent agent, used in refractory hypotension

Noradrenaline

Predominantly α-adrenergic agonist. Particularly useful in those with hypotension and a low SVR, e.g. septic shock

Dopamine

Low dose (1–3 μg/kg/min), predominantly acts on D1 receptor resulting in selective vasodilatation. Moderate dose – β1 receptors also stimulated with increased heart rate, myocardial contractility and cardiac output.
High dose (>10 μg/kg/min) – α-adrenergic effects predominant with an increase in SVR

Dopexamine

Dopamine analogue that activates β2 receptors as well as D1 and D2 receptors. Weakly positive inotrope and powerful splanchnic vasodilator, reducing afterload and improving blood flow to vital organs. Most useful in those with low cardiac output and peripheral vasoconstriction

Dobutamine

Predominantly β1 activity. Minimal α and β2 receptor activity results in vasodilatation. The net effect is increased cardiac output with decreased SVR

Milrinone and enoximone

Phosphodiesterase inhibitors with inotropic and vasodilator effects through non-adrenergic mechanisms

Vasopressin

Increases blood pressure and SVR. Used in septic shock where circulating levels of vasopressin are inappropriately low

α1-adrenergic receptors – located in vascular wall and heart. Increase SVR and duration of cardiac contraction
β1-adrenergic receptors – located in the heart, inotropic and chronotropic action results in increased cardiac output
β2-adrenergic receptors – located in blood vessels and mediate vasodilatation
Postsynaptic D1 receptors mediate vasodilatation of mesenteric, renal, coronary and cerebral circulation
Presynaptic D2 receptors cause vasoconstriction by inducing noradrenaline release

Specitic treatment of the cause In all cases the cause of shock must be identified if possible and specific treatment given when indicated:

■ Septic shock. Antibiotic treatment of septicaemia is discussed on page 16. Therapy should be directed towards the probable cause. In the absence of helpful clinical guidelines, ‘blind' intravenous antibiotic therapy (e.g. cefuroxime and gentamicin) should be started after perform-ing an infection screen: chest X-ray and culture of blood, urine and sputum. Lumbar puncture, ultrasonography and CT of the chest and abdomen are useful in selected cases. Abscesses require drainage. Recombinant human activated protein C and low dose hydrocortisone improves outcome in some patients with septic shock.

■ Anaphylactic shock must be identified and treated immediately (Emer-gency Box 12.1).

Monitoring

This is by both clinical and invasive means.

Clinical An assessment of skin perfusion, measurement of pulse, BP, JVP and urinary flow rate will guide treatment in a straightforward case. Additional invasive monitoring will be required in seriously ill patients who do not respond to initial treatment.

Invasive

■ Blood pressure. A continuous recording is made with an intra-arterial cannula, usually in the radial artery.

■ Central venous pressure (CVP) is related to right ventricular end-diastolic pressure, which depends on circulating blood volume, venous tone, intrathoracic pressure and right ventricular function. CVP is measured by inserting a central venous catheter (CVC) often under ultrasound control, into the superior vena cava or right atrium via percutaneous puncture of a subclavian or internal jugular vein. The catheter is connected to a manometer system (for intermittent CVP readings) or transducer system (for continuous readings displayed on a monitor). CVP is measured in a supine patient by aligning the transducer with the mid axilla (level with the right atrium); the normal range is 5-10 cmH2O (mid axilla). Other landmarks are advocated and whichever is chosen should be used on subsequent occasions. An isolated CVP is of limited value; a trend of readings is much more significant and should be viewed in conjunction with other parameters, e.g. blood pressure and urine output. In shock, CVP may be normal, because in spite of hypovolaemia there is increased venous tone. A better guide to circulating volume is the response to a fluid challenge (Fig. 12.1). A CVC is also used to measure Central venous oxyhaemoglobin saturation (ScvO2).

■ Pulmonary artery catheters, also called Swan-Ganz catheters, measure cardiac output and the pulmonary artery occlusion pressure, which

Fig. 12.1 The effect on the central venous pressure of a rapid administration of a ‘fluid challenge' to patients with a CVP within the normal range. (From Sykes MK Venous pressure as a clinical indication of adequacy of transfusion. Annals of the Royal College ofSurgeons ofEngland 1963; 33: 185-197.)

reflects left atrial pressure. In theory this should help to guide circulatory resuscitation. However, they increase complications and have not been shown to improve outcome and less invasive techniques are increasingly preferred.

■ Cardiac output is measured using oesophageal Doppler ultrasonography and lithium dilution; cardiac output is also measured using transoesopha-geal echocardiography.

RESPIRATORY FAILURE

Respiratory failure occurs when pulmonary gas exchange is sufficiently impaired to cause hypoxaemia with or without hypercapnia. In practical terms, respiratory failure is present when the PaO2 is < 8 kPa (60 mmHg) or the PaCO2 is > 7 kPa (55 mmHg).

It can be divided into two types (Table 12.5):

■ Type 1 respiratory failure in which the Pao2 is low and the PaCO2 is normal or low. It is most commonly caused by diseases that damage lung tissue. The hypoxaemia is due to ventilation-perfusion mismatch or right-to-left shunts.

■ Type 2 respiratory failure in which the Pao2 is low and the PaCO2 is high is caused by alveolar hypoventilation.

Monitoring

Clinical Assessment should be made on the following criteria: tachypnoea, tachycardia, sweating, pulsus paradoxus, use of accessory muscles of res-piration, intercostal recession and inability to speak. Signs of carbon dioxide retention may be present, such as asterixis (coarse tremor), bounding pulse, warm peripheries and papilloedema.

Table 12.5 Causes of respiratory failure

Type 1

Type 2

Pulmonary oedema

COPD

Pneumonia

Life-threatening acute severe asthma

Acute severe asthma

Respiratory muscle weakness, e.g. GBS

Pneumothorax

Respiratory centre depression, e.g. with sedatives

COPD

Sleep apnoea

Pulmonary embolism

Chest wall deformities

Acute respiratory distress syndrome

Inhaled foreign body

Lung fibrosis

Right-to-left cardiac shunts

COPD, chronic obstructive puỉmonaiy disease; GBS, Guiỉỉain-Barré syndrome

Table 12.6 Normal values for arterial blood gases

pH

7.35-7.45

PaCO2

4.3-6.0 kPa

Pao2

10.5-14 kPa

Base excess

± 2 mmol/L

Hco3

22-26 mmol/L

O2 saturation

95-100%

Pulse oximetry Lightweight oximeters placed on an earlobe or finger can give a continuous reading of oxygen saturation by measuring the changing amount of light transmitted through arterial blood. The normal range is 95100%, but in general, if the saturation is greater than 90%, oxygenation can be considered to be adequate. Although simple and reliable, these instru-ments are not very sensitive to changes in oxygenation. They also give no indication of carbon dioxide retention.

Forced vital capacity (FVC) In patients with acute neuro-muscular prob-lems, e.g. Guillain-Barré syndrome and myasthenia gravis, FVC is used as a guide to deterioration. ITU admission is recommended when the FVC is less than 20 mL/kg, and typically intubation and ventilation are necessary when the FVC is less than 10 mL/kg.

Arterial blood gas analysis Analysis of arterial blood gives definitive measurements of Pao2, PaCO2, oxygen saturation, pH and bicarbonate. Normal values are given in Table 12.6. In type 2 respiratory failure, retention of

carbon dioxide causes PaCO2 and [H+] to rise, resulting in respiratory acidosis. In chronic type 2 failure (chronic obstructive pulmonary disease (COPD), chest wall deformities) the bicarbonate concentration is also raised secondary to renal retention and the pH may partially or completely normalize due to this metabolic compensation (see Fig. 8.5). In type 1 respiratory failure or in hyperventilation there may be a fall in PaCO2 and [H+], resulting in respiratory alkalosis. Other abnormalities of acid-base balance are discussed on page 343.

Capnography This allows the continuous breath-by-breath analysis of expired carbon dioxide concentrations and is mandatory in patients having tracheal intubation outside the ITU.

Management

This includes the administration of supplemental oxygen, control of secre-tions, treatment of pulmonary infection, control of airway obstruction and limiting pulmonary oedema. Correction of abnormalities which may lead to respiratory muscle weakness, e.g. hypokalaemia, hypophosphataemia and undernutrition, is also necessary. In most patients oxygen is given by a face mask or nasal cannulae. With these devices, inspired oxygen concentration varies from 35 to 55%, with flow rates between 6 and 10 L. However, in patients with chronically elevated carbon dioxide (e.g. COPD), hypoxia rather than hypercapnia maintains the respiratory drive, and thus fixed-performance masks (e.g. Venturi masks) should be used, in which the concentration of oxygen can be accurately controlled. Respiratory stimulants such as doxa-pram have a very limited role in treatment.

Respiratory support Respiratory support is necessary when the above measures are not sufficient. The type depends on the underlying disorder and its clinical severity. Consideration should be given to ventilating patients with severe chronic lung disease, as those who are severely incapacitated may be difficult to wean from the ventilator:

■ Continuous positive airway pressure (CPAP) is used for acute type 1 respiratory failure. Oxygen is delivered to the spontaneously breathing patient under pressure via a tightly fitting face mask (non-invasive positive-pressure ventilation, NIPPV) or endotracheal tube. Oxygenation and vital capacity improve and the lungs become less stiff.

■ Bilevel positive airway pressure (BiPAP) provides assistance during the inspiratory phase and prevents airway closure during the expiratory phase. The main indication for BiPAP in the emergency setting is an acute exacerbation of COPD in patients who do not require immediate intubation and ventilation. In these patients it is indicated when there is a persistent decompensated respiratory acidosis (pH < 7.35 and PaCO2 > 6 kPa) fol-lowing immediate maximum medical treatment on controlled oxygen for no more than 1 hour (p. 521). BiPAP reduces the need for intubation, mortality and hospital stay. It is given for as long as possible during the first 24 hours and continued until the acute exacerbation has resolved, usually 2-3 days. Contraindications are facial burns/trauma/recent facial or upper airway surgery, vomiting, fixed upper airway obstruction, undrained pneumothorax, inability to protect the airway, intestinal obstruction, confusion, agitation and patient refusal of treatment.

■ Intermittent positive-pressure ventilation (IPPV). IPPV requires tracheal intubation and therefore anaesthesia if the patient is conscious. The indications for mechanical ventilation are listed in Table 12.7. The benefi-cial effects include improved carbon dioxide elimination, improved oxy-genation, and relief from exhaustion as the work of ventilation is removed. High concentrations of oxygen (up to 100%) may be administered accu-rately. If adequate oxygenation cannot be achieved, a positive airway pressure can be maintained at a chosen level throughout expiration by attaching a threshold resistor valve to the expiratory limb of the circuit. This is known as positive end-expiratory pressure (PEEP), and its primary

Table 12.7 Indications for IPPV

Indication

Comment

Acute respiratory failure

With signs of severe respiratory distress despite maximal therapy:
respiratory rate > 40/min
inability to speak
patient exhausted, confused or agitated

  Rising PaCO2 > 8 kPa
  Extreme hypoxaemia < 8 kPa, despite oxygen therapy

Acute ventilatory failure, e.g. myasthenia gravis,

Institute when vital capacity fallen to 10-15 mL/kg

Guillain-Barré syndrome

High PaCO2, particularly if rising, is an indication for urgent mechanical ventilation

Prophylactic postoperative ventilation

In poor-risk patients

Head injury

With acute brain oedema. Intracranial pressure is decreased by elective hyperventilation as this reduces cerebral blood flow

Trauma

e.g. Chest injury and lung contusion

Severe left ventricular failure

Coma with breathing difficulties

e.g. Following drug overdose

effect is to re-expand underventilated lung areas, thereby reducing shunts and increasing PaO2

■ Intermittent mandatory ventilation (IMV). This technique allows the ven-tilated patient to breathe spontaneously between mandatory tidal volumes delivered by the ventilator. These coincide with the patient's own respira-tory effort. It is used as a method of weaning patients from artificial ventilation, or as an alternative to IPPV.

The major complications of intubation and assisted ventilation are:

■ Trauma to the upper respiratory tract from the endotracheal tube

■ Secondary pulmonary infection

■ Barotrauma- overdistension of the lungs and alveolar rupture may present with tension pneumothorax (p. 561) and surgical emphysema

■ Reduction in cardiac output - the increase in intrathoracic pressures during controlled ventilation impedes cardiac filling and lowers cardiac output

■ Abdominal distension due to intestinal ileus - cause not known

■ Increased ADH and reduced atrial natriuretic peptide secretion. Together with a fall in cardiac output and reduced renal perfusion this leads to salt and water retention.

ACUTE LUNG INJURY/ACUTE RESPIRATORY DISTRESS SYNDROME

Acute lung injury (ALI) and the more severe acute respiratory distress syn-drome (ARDS) are defined as respiratory distress occurring with stiff lungs, diffuse bilateral pulmonary infiltrates, refractory hypoxaemia, in the presence of a recognized precipitating cause and in the absence of cardiogenic pul-monary oedema (i.e. no clinical evidence of left atrial hypertension).

Aetiology

The commonest precipitating factor is sepsis. Other causes include trauma, burns, pancreatitis, fat or amniotic fluid embolism, aspiration pneumonia or cardiopulmonary bypass.

Pathophysiology

The cardinal feature is pulmonary oedema as a result of increased vascular permeability caused by the release of inflammatory mediators. Oedema may induce vascular compression resulting in pulmonary hypertension, which is later exacerbated by vasoconstriction in response to increased autonomic nervous activity. A haemorrhagic intra-alveolar exudate forms, which is rich in platelets, fibrin and clotting factors. This inactivates surfactant, stimulates inflammation and promotes hyaline membrane formation. These changes may result in Progressive pulmonary fibrosis.

Clinical features

Tachypnoea, increasing hypoxia and laboured breathing are the initial fea-tures. The chest X-ray shows diffuse bilateral shadowing, which may progress to a complete ‘white-out'.

Management

This is based on the treatment of the underlying condition. Pulmonary oedema should be limited with fluid restriction, diuretics and haemofiltration if these measures fail. Aerosolized surfactant, inhaled nitric oxide and aero-solized prostacyclin are experimental treatments whose exact role in the management of ARDS is unclear. Repeated positional change, i.e. changing the patient from supine to prone may allow reductions in airway pressures and the inspired oxygen fraction in those with severe hypoxaemia.

Prognosis

Although the mortality has fallen over the last decade, it remains at 30-40%, with most patients dying from sepsis. The prognosis is very dependent on the underlying cause, and rises steeply with age and with the development of multiorgan failure.

Ebook Essentials of Kumar and Clark's Clinical Medicine, 5e

1. Ethics and communication

Ethics and communication

2. Infectious diseases

Infectious diseases

3. Gastroenterology and nutrition

Gastroenterology and nutrition

4. Liver, biliary tract and pancreatic disease

Liver, biliary tract and pancreatic disease
LIVER BIOCHEMISTRY AND LIVER FUNCTION TESTS
SYMPTOMS AND SIGNS OF LIVER DISEASE
JAUNDICE
HEPATITIS
NON - ALCOHOLIC FATTY LIVER DISEASE (NAFLD)
CIRRHOSIS
COMPLICATIONS AND EFFECTS OF CIRRHOSIS
LIVER TRANSPLANTATION
TYPES OF CHRONIC LIVER DISEASE AND CIRRHOSIS
PRIMARY SCLEROSING CHOLANGITIS
BUDD - CHIARI SYNDROME
LIVER ABSCESS
LIVER DISEASE IN PREGNANCY
LIVER TUMOURS
GALLSTONES
THE PANCREAS
CARCINOMA OF THE PANCREAS
NEUROENDOCRINE TUMOURS OF THE PANCREAS

5. Haematological disease

Haematological disease
ANAEMIA
Assessment and treatment of suspected neutropenic sepsis
HAEMOLYTIC ANAEMIA
INHERITED HAEMOLYTIC ANAEMIAS
ACQUIRED HAEMOLYTIC ANAEMIA
MYELOPROLIFERATIVE DISORDERS
THE SPLEEN
BLOOD TRANSFUSION
THE WHITE CELL
HAEMOSTASIS AND THROMBOSIS
THROMBOSIS
THERAPEUTICS

6. Malignant disease

Malignant disease
MYELOABLATIVE THERAPY AND HAEMOPOIETIC STEM CELL TRANSPLANTATION
THE LYMPHOMAS
THE PARAPROTEINAEMIAS
PALLIATIVE MEDICINE AND SYMPTOM CONTROL

7. Rheumatology

Rheumatology
COMMON INVESTIGATIONS IN MUSCULOSKELETAL DISEASE
COMMON REGIONAL MUSCULOSKELETAL PROBLEMS
BACK PAIN
OSTEOARTHRITIS
INFLAMMATORY ARTHRITIS
THE SERONEGATIVE SPONDYLOARTHROPATHIES
Clinical features, Investigations
INFECTION OF JOINTS AND BONES
AUTOIMMUNE RHEUMATIC DISEASES
SYSTEMIC INFLAMMATORY VASCULITIS
DISEASES OF BONE
THERAPEUTICS

8. Water, electrolytes and acid–base balance

WATER AND ELECTROLYTE REQUIREMENTS
BODY FLUID COMPARTMENTS
REGULATION OF BODY FLUID HOMEOSTASIS
PLASMA OSMOLALITY AND DISORDERS OF SODIUM REGULATION
DISORDERS OF POTASSIUM REGULATION
DISORDERS OF MAGNESIUM REGULATION
DISORDERS OF ACID - BASE BALANCE
THERAPEUTICS

9. Renal disease

Renal disease
INVESTIGATION OF RENAL DISEASE
GLOMERULAR DISEASES
NEPHROTIC SYNDROME
URINARY TRACT INFECTION
TUBULOINTERSTITIAL NEPHRITIS
HYPERTENSION AND THE KIDNEY
RENAL CALCULI AND NEPHROCALCINOSIS
URINARY TRACT OBSTRUCTION
ACUTE RENAL FAILURE/ACUTE KIDNEY INJURY
CHRONIC KIDNEY DISEASE
RENAL REPLACEMENT THERAPY
CYSTIC RENAL DISEASE
TUMOURS OF THE KIDNEY AND GENITOURINARY TRACT
DISEASES OF THE PROSTATE GLAND
TESTICULAR TUMOUR
URINARY INCONTINENCE

10. Cardiovascular disease

COMMON PRESENTING SYMPTOMS OF HEART DISEASE
INVESTIGATIONS IN CARDIAC DISEASE
CARDIAC ARRHYTHMIAS
HEART FAILURE
ISCHAEMIC HEART DISEASE
RHEUMATIC FEVER
VALVULAR HEART DISEASE
PULMONARY HEART DISEASE
MYOCARDIAL DISEASE
CARDIOMYOPATHY
PERICARDIAL DISEASE
SYSTEMIC HYPERTENSION
ARTERIAL AND VENOUS DISEASE
ELECTRICAL CARDIOVERSION
DRUGS FOR ARRHYTHMIAS
DRUGS FOR HEART FAILURE
DRUGS AFFECTING THE RENIN - ANGIOTENSIN SYSTEM
NITRATES, CALCIUM - CHANNEL BLOCKERS AND POTASSIUM - CHANNEL ACTIVATORS

11. Respiratory disease


Respiratory disease
TUBERCULOSISnd
DIFFUSE DISEASES OF THE LUNG PARENCHYMA
OCCUPATIONAL LUNG DISEASE
CARCINOMA OF THE LUNG
DISEASES OF THE CHEST WALL AND PLEURA
DISORDERS OF THE DIAPHRAGM

12. Intensive care medicine

Intensive care medicine

13. Drug therapy, poisoning, and alcohol misuse

Drug therapy, poisoning, and alcohol misuse

14. Endocrine disease

Endocrine disease
PITUITARY HYPERSECRETION SYNDROMES
THE THYROID AXIS
MALE REPRODUCTION AND SEX
FEMALE REPRODUCTION AND SEX
THE GLUCOCORTICOID AXIS
THE THIRST AXIS
DISORDERS OF CALCIUM METABOLISM
DISORDERS OF PHOSPHATE CONCENTRATION
ENDOCRINOLOGY OF BLOOD PRESSURE CONTROL
DISORDERS OF TEMPERATURE REGULATION
THERAPEUTICS

15. Diabetes mellitus and other disorders of metabolism

DIABETES MELLITUS
DIABETIC METABOLIC EMERGENCIES
COMPLICATIONS OF DIABETES
SPECIAL SITUATIONS
HYPOGLYCAEMIA IN THE NON - DIABETIC
DISORDERS OF LIPID METABOLISM
THE PORPHYRIAS

16. The special senses

THE EAR
THE NOSE AND NASAL CAVITY
THE THROAT
THE EYE

17. Neurology

COMMON NEUROLOGICAL SYMPTOMS
COORDINATION OF MOVEMENT
THE CRANIAL NERVES
COMMON INVESTIGATIONS IN NEUROLOGICAL DISEASE
UNCONSCIOUSNESS AND COMA
STROKE AND CEREBROVASCULAR DISEASE
EPILEPSY AND LOSS OF CONSCIOUSNESS
NERVOUS SYSTEM INFECTION AND INFLAMMATION
HYDROCEPHALUS
HEADACHE, MIGRAINE AND FACIAL PAIN
SPINAL CORD DISEASE
DEGENERATIVE NEURONAL DISEASES
DISEASES OF THE PERIPHERAL NERVES
MUSCLE DISEASES
MYOTONIAS
DELIRIUM
THERAPEUTICS

18. Dermatology

Dermatology

KEYWORD : Phác Đồ Chữa Bệnh, Bệnh Viện Bạch Mai, Từ Dũ , 115, Bình Dân, Chấn thương chỉnh hình, Chợ Rẫy, Đại học Y Dược, Nhân Dân Gia Định, Hoàn Mỹ, Viện Pasteur, Nhi Đồng Ung bướu, Quân Đội 103, 108,Phụ Sản Trung Ương, Bộ Y Tế,Phòng Khám, Hà Nội, Hải Dương, Thái Bình, Hồ Chí Minh, Sài Gòn, Đà Nẵng, Huế, Vinh, Đồng Nai, Bình Dương, Hải Phòng, Quảng Ninh, Hiệu Quả Cao, Chữa Tốt, Khỏi Bệnh, Là Gì, Nguyên Nhân, Triệu Chứng, Ăn Uống, Cách Chữa, Bài Thuốc
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