Care of the critically ill surgical patient

Published on 11/04/2015 by admin

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3 Care of the critically ill surgical patient

Introduction

The term ‘critical illness’ describes the condition of a patient who has a likely, imminent or established requirement for organ support; in simple terms where death is possible without timely and appropriate intervention. Some patients are at greater risk of developing critical illness than others (Box 3.1). Also certain conditions bring a likelihood of severe physiological stress (Box 3.2). It is unfortunately commonplace for the junior surgeon to be faced with a critically ill surgical patient, in various situations-from the peritonitic teenager admitted to A&E to the elderly postoperative hip replacement on HDU. It is crucial that a systematic approach is taken to assessment and treatment.

While it is more challenging to manage the patient with multiple organ failure it is rarely rewarding; rescuing the elderly post-laparotomy patient from cardiac failure brought about by fast atrial fibrillation is far harder than anticipating the hypokalaemia (causing the cardiac irritability) associated with ileus: prediction and prevention is essential. Prediction can begin with pre-operative assessment (such as identifying chronic airways disease or poor nutritional state) but continues through knowledge of the common problems associated with the condition/operation (such as the risk of chest infection after laparotomy). Prevention encompasses specific steps such as adequate replacement of fluid and electrolytes, adequate analgesia, chest physiotherapy and thromboprophylaxis, but the role of regular review (e.g. ward rounds) cannot be overstated.

Conversely a failure to assess patients regularly, to identify and act upon abnormal findings, to check whether one’s interventions have been carried out and whether they have been effective/sufficient, will make successful management less likely.

Finally, communication has become ever more important. The maxim ‘if it’s not in the notes it didn’t happen’ is not only for the benefit of the medical defence unions but reminds us that colleagues rely heavily on written information, not only if the case is complex but especially if the author is not available to discuss the case in person. The junior surgeon will often be working shifts and be responsible for many patients, in different clinical areas and will also have to leave the hospital at the end of his/her shift. Continuity of care relies entirely on this written ‘handover’ information. A schematic is suggested in Box 3.3.

Immediate management

There are two broad clinical scenarios facing the surgeon in critical care management: those patients who are ‘unstable’ (newly arrived or recently deteriorated on the ward) and those who are more ‘stable’ (typically on HDU/ITU with organ support established). Even in such a place of relative safety, ‘stable’ patients can become destabilised; the approach, even on the HDU/ITU ward round, should be structured as for the ‘unstable’ patient. This also assists the creation of an ordered management plan for the rest of the shift.

Unfortunately the junior surgeon is faced more often, as the attending doctor, with an unstable patient and there is a need to identify what is going on at the same time as institution of resuscitative measures (see Table 3.1). The mnemonic ABCDE is used as an aide-memoire for this systematic approach to the initial phase of critical care management, ‘immediate assessment and treatment’. By the end of this phase some common steps should have occurred:

Table 3.1 The ABCDE approach to the ill patient

Observe Examine Treat
Airway

Breathing Circulation Dysfunction   Expose  

It is essential to reassess the patient regularly to ensure that some measure of improvement has occurred and that time has been bought for a more thorough ‘full assessment’.

Common critical care problems

Although they may overlap in the severely ill surgical patient, there are common clinical scenarios that may occur. While it is worth considering these separately, by adopting a systematic approach, the assessment and management of the patient (along with a sound understanding of physiology) in most situations is straightforward.

Respiratory failure

This is the commonest cause of admission to an intensive care unit. Respiratory failure may be indicated by (ABCDE):

Immediate management (assuming patent airway) is to sit the patient upright and to institute high-flow oxygen therapy, exclude easily-reversible causes of respiratory distress (eg tension pneumothorax) and complete the ABCDE.

Alongside baseline investigations, the full patient assessment will reveal what is the likely cause of the respiratory impairment (Table 3.2). The severity of impairment can be estimated by arterial blood gas measurement; alongside the CXR this is the most important investigation.

Table 3.2 Management of respiratory failure

  Management steps
Generic steps Humidified O2, sit-up, IV access, monitoring in a place of safety, ABG, ECG, CXR, bloods, senior help especially if likely to need respiratory support (CPAP, BIPAP) or definitive airway
Airway obstruction Relieve obstruction, adjunctive airway measures
Pulmonary oedema (including iatrogenic overload) Diuretics
Atelectasis Physiotherapy
Bronchial obstruction (acute/chronic) Nebulised bronchodilators
Pneumonia Antibiotics
Pulmonary embolus* Maintain high preload, anti-coagulate
Myocardial infarction Analgesia, ACS protocol
Pleural effusion Consider aspiration
ARDS Treat underlying cause**
Pneumothorax Chest drain (needle thoracocentesis if tension)
Anaemia Transfuse to 10 g/dL
Neurological dysfunction (e.g. sedation) Give antidote if available, e.g. naloxone for opiate overdose, ‘bag & mask’ if poor ventilation

* See Box 3.5.

** See Box 3.6.

Technically a patient is regarded as suffering respiratory failure if the arterial partial pressure of oxygen (PO2) is <8 kPa; a higher level of oxygen obtained on blood gas may still be seen if the patient has already been receiving supplementary oxygen. Respiratory failure is further divided into type 1 and type 2. The failure to oxygenate, despite adequate ventilation (with normal or even low CO2 levels), is termed type 1 respiratory failure; the failure to oxygenate because of inadequate ventilation (with high CO2 levels) is type 2.

In general terms, hypoxia improves with increases in the inhaled oxygen concentration. Predicting/identifying impaired ventilation is the next most crucial step; in hypercapnia measures must be taken to improve ventilation. There may be a significant pre-existing respiratory problem and there may be limits as to what can be achieved with standard ward care. In type 2 respiratory failure, merely increasing the inhaled oxygen concentration will improve arterial oxygenation (and buy time) but may paradoxically worsen the ventilatory drive (and lead to worsening CO2 levels, respiratory acidosis and confusion). Unless a readily-reversible factor is identified, the patient will require respiratory support (and often intubation) which usually necessitates asking for senior help.

Shock/circulatory failure

Shock is defined as the failure of the circulation to maintain adequate tissue perfusion. In immediate management (ABCDE), it is usually (but not always) associated with low systolic blood pressure (<100 mmHg) and tachycardia (HR >100); other signs vary according to the underlying cause. ‘Hard’ signs of reduced tissue perfusion include oliguria and metabolic acidosis. Immediate management may involve definitive treatment (e.g. control of external haemorrhage or the need to follow the advanced life support pathway) but the common generic steps are:

Full assessment

Clinical assessment (and data gathered from charts and the notes) will usually point to a typical cause (Box 3.7), but should begin by a targeted examination to establish the likely form of shock. Warm peripheries will point to a ‘distributive’ shock; that is to say where there is a failure of peripheral resistance (BP= (HR × CO) × TPR). This usually indicates systemic inflammatory response ± sepsis, but may occur in anaphylaxis or ‘neurogenic shock’ (such as spinal cord transection). Cool peripheries with signs of reduced circulating volume (low JVP, signs of dehydration, obvious fluid losses) may point to hypovolaemic shock. Cool peripheries and high JVP suggest a ‘pump failure’ – this may be intrinsic ‘cardiogenic shock’ if there has been a cardiac event (MI, arrhythmia) but can also occur secondarily to extrinsic compromise (‘obstructive shock’), tension pneumothorax, cardiac tamponade or pulmonary embolism (Table 3.3).

Further definitive management depends on the exact cause and any easily reversible causes should take priority. The movement of the patient to a critical care area and the institution of invasive monitoring is invariably required, as established shock is not often rapidly reversible. Hypovolaemic states require expansion of circulating volume (to replace losses; see Chapter 4); low peripheral resistance states also require fluid replacement (as the circulating volume requirement increases) but often require inotropic support to increase arteriolar tone (see SIRS/sepsis below). Pump failure situations may require a combination of careful pre- and after-load management and in the case of cardiogenic shock, management is very difficult requiring expert cardiological input. For management of anaphylaxis see Box 3.8.

Sepsis and multi-organ failure

The body’s response to threat of injury or infection is complex, involving multiple mediators (e.g. TNF, IL-1) to co-ordinate the inflammatory response. There is clearly a balance struck between pro- and anti-inflammatory mediators, and if the inflammatory response is excessive the process may ultimately harm the patient, with the development of a shock state and progressing to multi-organ failure. A continuum exists between the mild derangement of SIRS through to septic shock (Box 3.9). Certain conditions seem to predispose to an inflammatory response (Box 3.10) but there are probably other factors that determine outcome – including the severity of the insult, the delay to treatment and the underlying patient substrate (pre-existing cardiac, respiratory or renal impairment). Early recognition, immediate resuscitation and identification and treatment of any underlying cause are the key steps in management. If an infective source is suspected, prompt antibiotic administration is crucial pending more definitive treatment (e.g. drainage of abscess).

Renal failure (Box 3.11)

Low urine output is one of the commonest reasons a doctor is called to review a surgical patient. Unfortunately one of the body’s natural responses to stress is to reduce urine output, and working out when a patient is appropriately concentrating his urine rather than sliding into acute renal failure can present a challenge.

Renal dysfunction is however a common complication in the critically ill, and a major reason for admission to the ICU. The patients’ baseline renal (dys)function is a major risk factor. A baseline creatinine of >140 mmol/L, although in numerical terms 15% above normal (range usually 125 mmol/L or less) represents as much as 80% loss of renal function. These patients should be carefully monitored as there is a much greater chance that the chronicallly-impaired kidney will fail in critical illness.

The key management steps when asked to see a patient with low urine output (<0.5 mL/kg/hr) are as follows:

Although it is crucial to watch out for the complications of established renal failure (and know how to treat – see Table 3.4) these usually take a little time to develop. Fluid overload, hyperkalaemia and metabolic acidosis are easily identified by these initial steps.

Table 3.4 Complications of acute renal failure (and indications for dialysis)

Complication Manifestation
Hyperkalaemia Cardiac arrhythmia
Fluid overload Pulmonary oedema, respiratory failure
Metabolic acidosis Coma, arrhythmias, cardiac failure
Uraemia Encephalopathy, pericariditis, gastrointestinal bleeding

Emergent treatment of hyperkalaemia (>6.5 mmol/L and/or ECG changes).

Calcium gluconate (10 mL of 10%), repeat if ECG changes unchanged at 5 min.

Insulin 10 U with 50 mL 50% dextrose over 15–30 min.

(If acidotic) sodium bicarbonate solution get expert advice.

Salbutamol 5 mg nebulised.

What do you think the volaemic status (intravascular, i.e. hydration state) of the patient is? Clinical exam, charts, likely losses and knowledge of pre-existing conditions will all aid an educated guess. If any doubt that the patient is euvolaemic (i.e. adequately hydrated) continue fluid rehydration.

Can you be certain that there is no obstruction? Total anuria is an obstructed urinary system until proven otherwise. Request KUB ultrasound if any doubt.

Take a history – what has happened to the patient recently?

Standard courses of treatment are as follows. Sepsis – treat source as above. Jaundice (the danger of liver and kidney failure ‘the hepatorenal syndrome’) – relieve any obstructive cause. Nephrotoxic drugs (stop if possible). Rhabdomyolysis (muscle breakdown in trauma or limb ischaemia – myoglobin is nephrotoxic) – aggressive hydration and alkalinize urine.

If renal deterioration is not quickly reversed and it becomes likely that renal replacement therapy will be necessary, get specialist help (renal team, intensive care physician).

For cardiac complications, see Box 3.12.