17- Trouma & ER Refrence 2 Flashcards
1
Q
What are the signs of decreased tissue perfusion that can indicate shock?
A
Signs of decreased tissue perfusion in a shocked patient include cool peripheries, poor filling of peripheral veins, increased respiratory rate, increased core-peripheral temperature gradient, prolonged capillary refill time (>2 seconds), poor signal on pulse oximeter, poor urine output (<0.5 ml/kg body weight/h), anxiety and restlessness, decreased level of consciousness, and metabolic acidosis or raised serum lactate levels.
2
Q
What are some common causes of cardiogenic shock in surgical patients?
A
Myocardial infarction, acute arrhythmias, post-cardiac surgery myocardial ‘stunning,’ and cardiac contusions due to trauma
3
Q
What are the clinical features of cardiogenic shock?
A
Similar to hypovolemic shock, cardiogenic shock is characterized by cool clammy peripheries, reduced capillary return, reduced urine output, reduced level of consciousness, and elevation of cardiac filling pressure leading to pulmonary edema
4
Q
How can cardiogenic shock be diagnosed in a surgical patient?
A
A careful history and examination of the chest, heart sounds, and neck veins, along with assessment of a chest radiograph and ECG. Urgent echocardiography may be valuable if the diagnosis is unclear
5
Q
What are some clinical features of sepsis in the early stage?
A
Restlessness and slight confusion, tachypnea, tachycardia, vasodilation, high cardiac output, normal or slightly decreased systolic blood pressure, oliguria, metabolic acidosis, elevated blood lactate, warm, dry, suffused extremities
5
Q
What are the principal causes of obstructive shock?
A
Cardiac tamponade, tension pneumothorax, and pulmonary embolism
6
Q
What are the specific features of obstructive shock?
A
Restriction of heart function leading to a drop in cardiac output. Elevated JVP can be observed. Prompt intervention is needed to relieve pressure on the heart
7
Q
What are the specific features of septic shock?
A
In early sepsis, there may be a fall in systemic vascular resistance due to vasodilation, leading to an increase in cardiac output. Blood pressure may be well-maintained, and the patient may appear pink with flushed peripheries. In later stages, or if the patient is hypovolemic, blood pressure may fall and the patient may resemble someone with hypovolemic shock. Fluid loss due to increased capillary permeability and myocardial depressant factors contribute to hypotension. Oxygen and fluids are initially required, along with identification and treatment of the source of infection.
8
Q
What is the essential aim of treatment for sepsis?
A
Restoration of adequate perfusion at the cellular level
8
Q
What are some clinical features of sepsis in the late stage?
A
Decreased level of consciousness, tachypnea, tachycardia, low cardiac output, systolic blood pressure less than 80mmHg, oliguria, metabolic acidosis, elevated blood lactate, cold extremities
9
Q
What are the mainstays of early treatment for sepsis?
A
Infusion of fluid and administration of oxygen to improve cardiac output and oxygen transport
10
Q
How should patients with shock be initially treated if cardiogenic and obstructive forms of shock are not suspected?
A
Fluid administration with an initial bolus of 10ml/kg body weight of crystalloid if normotensive, or 20ml/kg body weight if hypotensive. Oxygen should be given initially in high flow
11
Q
What is the recommended size for a peripheral cannula for venous access?
A
At least one large-bore (16G) peripheral cannula
12
Q
Where is reliable venous access usually obtained from?
A
The antecubital fossa or via the cephalic vein at the wrist
13
Q
What can be done if vasoconstriction makes it difficult to obtain venous access?
A
A “cut-down” procedure can be performed in the antecubital fossa or on the long saphenous vein in front of the medial malleolus
14
Q
What should be done in profoundly shocked patients who cannot obtain initial access through peripheral veins?
A
Cannulate the femoral vein percutaneously in the groin
15
Q
What urgent tests should be conducted when obtaining venous access?
A
Cross-matching, haematology, and biochemistry tests
16
Q
Under what circumstances is a suprapubic catheter inserted?
A
When there is a possibility of urethral injury (as in severe pelvic fractures) or when dealing with young children
17
Q
How is a suprapubic catheter inserted?
A
Under ultrasound control once the bladder has filled
18
Q
How often should urine output be measured after bladder catheterization?
A
Hourly
18
Q
Where is a pulse oximeter typically attached?
A
To a finger or ear lobe
19
Q
How is a central venous catheter inserted?
A
Percutaneously via the internal jugular or subclavian veins
20
Q
What does a low or negative CVP indicate in a shocked patient?
A
The need for more fluid
21
Q
What does a very high CVP indicate in a shocked patient?
A
Right ventricular or biventricular failure and the need for diuretics, vasodilators, or inotropic agents, or an obstructive cause
21
What is the initial fluid management for shock?
Boluses of warmed crystalloid (up to 20 ml/kg body weight)
22
What influences the choice of fluid for initial replacement in shock?
The type of fluid lost
23
What should be monitored in the shocked patient?
Clinical appearance, respiratory rate, peripheral circulation, restlessness or confusion, pulse rate, capillary refill time, systemic blood pressure, hourly urine output, and CVP (if appropriate)
24
What additional information can be gained through monitoring in the shocked patient?
Blood urea and electrolyte concentrations, haemoglobin concentration, white cell count and haematocrit, ABGs including lactate level, pulse oximetry, core and peripheral temperature
25
What samples should be sent for bacteriological examination when sepsis is suspected?
Appropriate samples such as blood, urine, sputum, and drain fluids
26
Which are the most commonly used crystalloids for fluid resuscitation in shock?
Normal saline and Ringer's lactate solution
27
Why is Ringer's lactate preferred over normal saline for fluid resuscitation?
It can buffer metabolic acidosis and avoid hyperchloraemic acidosis
28
What is the theoretical risk of using Ringer's lactate in patients with acute kidney injury or chronic kidney disease?
Hyperkalaemia
29
What is the theoretical advantage of colloid infusions over crystalloids?
They are retained more in the intravascular space
30
Do studies show any benefit of colloid use over crystalloid use in clinical outcomes?
No, there is no significant benefit
31
What are the risks associated with colloid infusions?
Anaphylaxis, coagulopathy, and acute kidney injury
32
What are the potential effects of crystalloid resuscitation compared to colloid resuscitation?
Greater weight gain and tissue edema with crystalloid use
32
How much crystalloid is required to replace a given amount of blood loss compared to colloid?
Approximately three times the volume
33
Is there a fixed relationship between serum albumin concentration and colloid osmotic pressure?
No, except when serum albumin falls very low
34
Do both colloids and crystalloids pass through the vascular basement membrane in septic shock with increased capillary permeability?
Yes
35
What is the recommended volume limit of crystalloid used during resuscitation?
<50% of non-blood fluid infusion
36
What is one of the most important steps in managing shocked patients?
Assessing the response to treatment
37
How often should the patient's progress be reassessed during resuscitation?
At least every 30 minutes or so
38
What should be done if the patient's signs are not improving during resuscitation?
Change the plan of action and consider involving senior help if in doubt
39
What are the steps in the algorithm of cardiovascular monitoring/support?
1. Establish and maintain normovolaemia; 2. Assess response; 3. CVP assessment; 4. Invasive monitoring and inotropic treatment
40
What are some signs that surgical patients may present with in cardiovascular compromise?
Oliguria, hypotension, tachycardia, hypoxia, acidosis
41
What are the indicators of inadequate CVP?
CVP <8cmH2O
42
What should be done if CVP is inadequate but circulation is still inadequate?
Reassess the cause and treat as necessary, consider inotrope in a higher level of care
43
What should be done if CVP is high (>15cmH2O) and the patient exhibits signs of cardiac failure?
Treat simple LVF or suspect cardiogenic shock and call for help
44
What may be responsible for hypovolaemic shock that is refractory to fluid replacement and oxygen administration?
Underestimation of the degree of hypovolaemia, failure to arrest haemorrhage, cardiac tamponade or tension pneumothorax, underlying sepsis with inadequate source control, secondary cardiovascular effects due to delay in treatment
45
What are the essential metabolic monitoring parameters in refractory shock?
Urea and electrolyte levels, arterial pH, blood gas measurements, blood lactate levels
46
When should bicarbonate be considered for the treatment of acidosis in refractory shock?
If the patient's pH is very low (<7.1) and myocardial depression from acidosis may be contributing to the shock
46
What does the disappearance of metabolic acidosis indicate in the context of shock?
Adequate resuscitation and improved cardiac output
46
In what cases should patients with shock be managed in a critical care environment?
Severe trauma, sepsis, cardiogenic shock, or shock complicated by secondary myocardial dysfunction
47
What does respiratory acidosis with an increase in arterial PaCO2 indicate?
The need for endotracheal intubation and assisted ventilation
48
When may patients with shock require inotropic support?
Based on the underlying cause of shock and measurement of cardiovascular parameters, particularly confirmation of adequate circulatory volume
49
How is the selection of an inotropic agent determined?
Based on the cardiovascular effects of the drug and the underlying pathophysiology, particularly the drug's effect on adrenergic receptors
49
What are the benefits of using automated devices for non-invasive blood pressure measurements?
They can demonstrate trends in blood pressure and are reliable in most stable patients, as well as easy to use in a ward setting
50
What are some parameters that can be monitored in the cardiovascular system?
Blood pressure, CVP (central venous pressure), cardiac output or cardiac index (CI)
50
What is the priority in treating shock?
Restoring perfusion as a matter of urgency
51
What are the indications for intensive monitoring of the cardiovascular system?
Failure to restore and maintain cardiovascular homeostasis, procedures with rapid or profound changes in preload or afterload, treatment with vasoactive drugs, patients at risk of low perfusion state
51
What components of cardiac output can be monitored and manipulated?
Preload, cardiac function and compliance, afterload
52
What are some common standards for invasive monitoring methods?
Sound knowledge of relevant practical anatomy, competence in line insertion, explanation of the procedure to the patient, aseptic technique, knowledge of contraindications and complications, benefits outweighing risks
53
What are the commonly used anatomical sites for arterial pressure monitoring?
Radial artery (most frequent), dorsalis pedis artery
54
What can the shape of the arterial waveform indicate in normal and pathological conditions?
Systemic vascular resistance and cardiac contractility
54
What are the potential contraindications for cannulating the radial artery?
Local sepsis and coagulopathy
55
What components are connected to the arterial cannula for pressure monitoring?
Short length of rigid tubing, three-way tap, flush device, and transducer
55
What factors influence central venous pressure (CVP)?
Venous return, right heart compliance, intrathoracic pressure, and patient position
55
What are some complications associated with arterial cannulation?
Haematoma, thrombosis, distal ischemia, intimal damage, false aneurysm formation, disconnection, injection of irritant drugs
56
What is the recommended patient position for the infraclavicular subclavian route?
Tilted 20° head down, with arms by the side and head turned away from the entry side
57
How is the infraclavicular subclavian route typically performed?
Using ultrasound guidance for increased accuracy
58
Where should the catheter be advanced to?
A previously measured point so that the tip lies in the distal superior vena cava (SVC)
58
In which direction should the needle be advanced when performing the infraclavicular subclavian route?
Horizontally towards the suprasternal notch in a linear fashion
58
What should be done if the initial attempt is unsuccessful?
Systematically search with further straight insertions to locate the vein
58
Where should the cannula be inserted for this technique?
1-2cm below the midpoint of the clavicle
59
What is the ultrasound-guided approach for accessing the vein in the infraclavicular subclavian route?
Locating the vein at the medial border of sternomastoid, at the level of the thyroid cartilage, and anterolateral to the carotid artery
60
How should the artery be displaced during the ultrasound-guided approach?
Medially
61
In what direction should the needle be advanced when using ultrasound guidance for the infraclavicular subclavian route?
Inferiorly at a 30° angle to the skin, parallel to the artery but lateral towards the ipsilateral nipple
62
What does the UK National Institute for Health and Care Excellence (NICE) recommend for central venous catheter placement?
Using ultrasound imaging for guidance, especially in elective situations, and undergoing training in ultrasound use
63
When is ultrasound still recommended for emergency cases involving the subclavian route?
When poor visualization of the subclavian vein occurs behind the clavicle
64
Where is the best zero reference point for CVP measurement?
Midaxillary line at the fourth intercostal space, or the second intercostal space at the sternal edge
65
In which situations is CVP measurement indicated?
Fluid replacement therapy for hypovolaemia, monitoring the effect of vasoactive drugs, diagnosing right ventricular failure, administering potent drugs, and administering parenteral nutrition using a dedicated clean lumen
66
What are some factors that can lead to inaccurate CVP readings?
Failure of zeroing or calibration, placement of the cannula tip in the right ventricle, tricuspid regurgitation and incompetence, AV dissociation, and nodal rhythms
67
What are some complications associated with central line insertion?
Rupture of vessels and hemorrhage, local hematoma or hemothorax, tension pneumothorax, air embolism, extravascular catheter placement, catheter knotting or breakage, catheter misplacement, neurapraxia, arterial or lymphatic puncture, tracheobronchial puncture, and sepsis
67
What factors can cause a false impression of higher right ventricular filling pressure during CVP measurement?
Variations in intravascular volume, sympathetic tone, cardiac output, and intrathoracic pressure (especially during positive pressure ventilation)
68
What should be checked before using the CVP line and acting on measurements?
Easy aspiration of blood, pressure fluctuation with respiration, and confirmation of line position by X-ray
69
How can systemic vascular resistance (SVR) be estimated using cardiac output?
By using the equation: Cardiac output = (mean arterial pressure (MAP) - CVP) / systemic vascular resistance
70
Why has the use of pulmonary artery catheters decreased in general critical care units and theaters?
Due to high invasiveness, significant risk of serious complications, and the availability of less invasive cardiac output monitors
71
What are some less invasive techniques for measuring cardiac function?
Trans-oesophageal Doppler (TOD), echocardiography, pulse contour cardiac output with indicator dilution (PiCCO), and the LiDCOTM (lithium dilution cardiac output) system
72
How does trans-oesophageal Doppler (TOD) measure blood velocity?
By using the Doppler shift principle to measure blood velocity in the descending aorta using a disposable Doppler probe passed down the oesophagus
73
What information can be obtained from the waveform displayed by TOD?
Information on preload, stroke volume, and afterload
74
How is stroke volume calculated using TOD?
By determining the area under the curve of the waveform and applying a factor based on the patient's age, height, and weight
75
What is the disadvantage of TOD?
The patient must be anesthetized and intubated, and the technique is operator dependent and cannot be used in certain conditions or surgical procedures
76
What is the role of echocardiography in critically ill patients?
Assessment of preload and cardiac contractility, diagnosis of major cardiac structural abnormalities, and evaluation of inferior vena cava size for patient filling
77
What is PiCCO and how does it calculate cardiac output?
PiCCO is a method that calculates cardiac output using a peripheral arterial cannula. It provides beat-to-beat information to a computer, which analyzes the heart rate and pressure waveform to determine the area under the curve. The method is improved by using a sensitive thermistor in the cannula for thermodilutional calibration.
78
What are some limitations of PiCCO?
PiCCO requires regular recalibration and can become unreliable when the arterial waveform is suboptimal, such as with a kinked line or the presence of air or blood clots.
78
What is LiDCO and how does it measure cardiac output?
LiDCO is a technique that uses the injection of lithium chloride into a central vein, with the lithium concentration analyzed using an ion-sensitive electrode. Blood samples can be taken from a normal peripheral arterial line. Continuous pulse contour analysis is combined with lithium dilution for measuring cardiac output.
79
How does thermodilution measurement work in PiCCO?
A small drop in the temperature of arterial blood follows the injection of ice-cold saline into a central vein. The magnitude of temperature change is proportional to cardiac output. This thermodilution measurement is used to calibrate the continuous cardiac output monitoring software in PiCCO.
80
What are some factors that can interfere with the analysis of lithium concentration in LiDCO?
Some muscle relaxants, like atracurium, can interfere with the analysis of lithium concentration. Additionally, lithium is contraindicated in certain patients, such as pregnant women.
81
Which drugs are commonly used as inotropes?
The most commonly used inotropes are adrenaline and dobutamine.
82
What is the specific use of noradrenaline in septic shock?
Noradrenaline is used as a vasopressor in septic shock to increase and maintain systemic vascular resistance (SVR) within the normal range.
83
When are vasodilators such as sodium nitroprusside or nitrates used?
Vasodilators are used when pulmonary edema occurs in heart failure. However, they can cause a reflex tachycardia if the blood pressure falls.
84
In what situations are combinations of inotropes and vasodilators or inotropes and vasoconstrictors used?
Combinations of inotropes and vasodilators may be used, such as adrenaline and nitroglycerine in severe left ventricular failure (LVF). Combinations of inotropes and vasoconstrictors, like dobutamine and noradrenaline, may be used in severe sepsis.
85
What precautions should be taken when using inotropes and vasodilators?
Inotropes and vasodilators should only be used when a full range of monitoring is available and should not be used on ordinary surgical wards or in the presence of hypovolemia. The specific dose ranges and modes of delivery for these drugs are beyond the scope of this course.
86
What is the role of a surgical trainee in caring for patients who require inotropes and vasodilators?
The role of a surgical trainee is to recognize the clinical conditions that require the use of inotropes and vasodilators and refer the patient to the appropriate level of monitoring and care.
86
What should the surgical team be aware of when treating AKI?
The life-threatening complications of AKI, such as hyperkalemia and pulmonary edema
87
What is one of the most common reasons why a surgical team may be called to see a patient?
Poor urine output
88
What are the five points to consider in the development of acute kidney injury (AKI) in surgical patients?
The kidneys require adequate perfusion, renal perfusion depends on blood pressure, surgical patients with poor urine output may need more fluid, absolute anuria is usually caused by urinary tract obstruction, and diuretics are not initially used to treat poor urine output in surgical patients
89
How is acute kidney injury (AKI) defined?
AKI is a biochemical diagnosis characterized by an acute increase in serum creatinine due to injury or an inability to excrete waste products
90
What is the current classification system for AKI?
The Acute Kidney Injury Network (AKIN) classification system
91
What are the three clinical scenarios recognized as AKI?
An abrupt reduction in kidney function, a percentage increase in serum creatinine level, or a reduction in urine output
92
What are the three main categories of AKI etiology?
Prerenal, intrinsic renal, and post-renal
93
Which is the most common etiology of AKI in surgical patients?
Prerenal failure
94
What is acute tubular necrosis (ATN)?
ATN is a condition that can result from prerenal failure and is characterized by the death of kidney tubular cells
95
What is the cause of post-renal failure?
Obstruction and back-pressure in the urinary tract
95
What are the urine output criteria for Stage 2 AKI?
Urine output of <0.5 ml/kg/h over 12 hours
96
What are the GFR criteria for Stage 1 AKI?
An increase in creatinine of >26.4μmol/L or 1.5- to 2.0-fold from baseline
97
What are the urine output criteria for Stage 1 AKI?
Urine output of <0.5 ml/kg/h over 6 hours
97
What are the GFR criteria for Stage 2 AKI?
An increase in creatinine of 2- to 3-fold from baseline
98
What are the GFR criteria for Stage 3 AKI?
An increase in creatinine of 3-fold from baseline or serum creatinine >354μmol/L
99
What are the urine output criteria for Stage 3 AKI?
Urine output of <0.3 ml/kg/h over 24 hours
100
What are the common causes of prerenal AKI?
Hypovolemia, sepsis, and low cardiac output
101
What are the common causes of intrinsic renal AKI?
Acute tubular necrosis, ischaemic injury, nephrotoxic injury, abdominal compartment syndrome, and hepatorenal syndrome
102
What are the common causes of post-renal AKI?
Bladder outflow obstruction and bilateral ureteric obstruction
103
What measures can be taken to identify and protect patients at risk of perioperative renal dysfunction?
Delaying surgery if necessary, investigating the cause of pre-existing renal impairment, reviewing drug therapy, considering the effects of nephrotoxins, and seeking the opinion of a renal physician
104
What should be considered in terms of fluid balance and cardiovascular status in perioperative management to protect renal function?
Optimum perioperative fluid balance, optimization of cardiovascular status (especially in terms of volume), and avoiding hypotension and hypovolemia
105
What investigations can be conducted to assess renal function in patients at risk?
Urinalysis, renal ultrasound, and more detailed tests such as a MAG3 scan
106
What should be done in the emergency setting to prevent renal dysfunction?
Strict attention to fluid balance, maintenance of optimum cardiac output, avoidance of nephrotoxic drugs, aggressive management of sepsis, and regular review of patients at risk
107
What are the key aspects of management for acute kidney injury (AKI)?
Recognition and correction of respiratory and circulatory problems, immediate identification and management of life-threatening consequences of renal impairment, exclusion of urinary tract obstruction, careful search for and correction of the underlying cause, and seeking early help from appropriate specialists
108
What should be assessed regarding intravascular volume in a patient with AKI?
Thorough and repeated assessment of intravascular volume, considering signs of hypovolemia and fluid overload, such as hypotension, elevated blood pressure, raised JVP/CVP, peripheral and pulmonary edema, ascites, and effusions
108
What should be done if a patient with AKI presents with complete anuria?
Exclude urinary tract obstruction until proven otherwise
109
What investigations should be conducted for acute kidney injury?
Dipstick urinalysis, urine biochemistry and microbiology, renal ultrasound scan, plain chest X-ray (for pulmonary edema), and further radiological investigations as necessary (with consultation with seniors) such as CT and radionucleotide studies
110
What blood tests should be conducted to complement routine biochemistry analysis in the management of acute kidney injury (AKI)?
Full blood count (FBC) to detect anaemia and infection, routine biochemistry including urea, creatinine, and potassium levels, liver function tests (LFTs) to recognize hepatorenal syndrome, calcium phosphate levels if malignancy, rhabdomyolysis, or tumor lysis is suspected, creatine kinase to detect rhabdomyolysis, C-reactive protein as a measure of infection and/or inflammation, arterial blood gas (ABG) and lactate levels to assess hypoxia, acidosis, and tissue/organ ischemia
111
What are the main treatment goals for AKI?
To restore and maintain renal perfusion, relieve any obstruction, oxygenate the tubules, remove/avoid toxins, and identify and treat any underlying cause
112
What is the recommended approach to restore renal perfusion in AKI patients?
Aim to restore euvolaemia using balanced salt solutions and ensure regular monitoring of cardiovascular parameters, including urine output. Once euvolaemia is achieved, give maintenance fluid to match urine output and any ongoing hourly losses. Invasive cardiovascular monitoring may be required if circulating volume is not rapidly restored
112
How can prerenal causes be distinguished from intrinsic renal problems due to acute tubular necrosis (ATN)?
Prerenal pathology typically retains the concentrating ability of the tubular system, producing urine with high osmolarity, high urea and creatinine, and low sodium concentration. ATN results in low osmolar urine with high sodium and low urea/creatinine levels
113
What should be done to exclude post-renal obstruction in AKI patients?
Perform ultrasonography to exclude post-renal obstruction and treat accordingly
114
How can acute and chronic renal problems be distinguished?
Ultrasound may reveal small kidneys (<9cm) with echo-bright parenchyma, suggesting chronic damage. Acutely injured but normal kidneys will be echo-bright due to edema but will be of normal size and are more likely to recover. Acute on chronic renal failure is less likely to recover
115
What measures should be taken to oxygenate the tubules in AKI management?
Give oxygen and maintain a saturation of greater than 94%. Ensure that the hemoglobin level is greater than 70g/L
116
What should be done to exclude toxins in the management of acute kidney injury (AKI)?
Review the drug chart and avoid nephrotoxins, including contrast medium. Common examples are aminoglycosides, NSAIDs, ACE inhibitors, and β-blockers. Adjust the doses of drugs excreted by the kidney, such as opioids, to prevent toxic side effects. Test for pigments like myoglobinuria and hemoglobinuria where appropriate.
117
What is rhabdomyolysis and how is it treated in AKI management?
Rhabdomyolysis is the breakdown of damaged muscle with the release of myoglobin into the circulation. It can occur after crush injuries, acute limb ischemia, prolonged surgery, or immobility. Treatment includes aggressive volume expansion and sodium bicarbonate to alkalinize the urine, promoting diuresis and reducing the negative effect of acid breakdown products of myoglobin on renal tubules. Early recognition and immediate treatment are crucial for success.
118
When is renal replacement therapy (RRT) indicated in AKI management?
RRT is indicated when acute kidney injury fails to respond to other measures.
119
What is the process of hemodialysis and how does it work?
Hemodialysis is a process in which low-molecular-weight solutes equilibrate between a blood compartment and a dialysate compartment separated by a semipermeable membrane. Solute waste moves across the membrane down a concentration gradient. Dialysis can be intermittent or continuous, with continuous methods preferred in critically ill patients.
120
What is haemofiltration and how does it differ from hemodialysis?
Haemofiltration involves the continuous convection of molecules across a permeable membrane. The fluid removed during haemofiltration is replaced with a buffered physiological solution. Haemofiltration is more effective in removing large quantities of fluid but less effective than dialysis in clearing smaller molecules. It is usually performed using a continuous veno-venous method, known as continuous veno-venous haemofiltration (CVVH). CVVH has the least risk of significant intravascular fluid shifts and hemodynamic instability, making it a preferred method for providing renal support in ICU patients.
121
What are the indications for initiating renal replacement therapy (RRT) in cases of uraemia?
The threshold for initiating RRT in uraemia is controversial and depends on the rapidity and absolute level of rise in urea, as well as the presence of symptoms. A rise above 35mmol/L unresponsive to other therapies is usually an absolute indication for RRT. The choice between dialysis and haemofiltration depends on the clinical circumstances.
122
What are the absolute indications for initiating renal replacement therapy (RRT) in cases of acute kidney injury (AKI)?
Refractory hyperkalemia (>6mmol/L), refractory pulmonary edema and fluid overload, and uremic encephalopathy
123
What are the relative indications for initiating renal replacement therapy (RRT) in cases of AKI?
Acidosis (pH <7.2), uraemia, pericarditis, and toxin removal
124
What is the immediate treatment for acute hyperkalemia (K+ above 6.5mmol/L) to prevent life-threatening cardiac dysrhythmia and arrest?
Immediate treatment includes identifying and stopping any underlying contributory cause, such as blood transfusions, drugs that reduce renal potassium excretion, or intravenous fluid containing potassium and potassium supplements. An ECG should be performed to assess for ECG changes associated with hyperkalemia. Emergency measures should be instituted to temporarily reduce K+ levels, including continuous cardiac monitoring, insulin with dextrose intravenously, sodium bicarbonate intravenously, calcium gluconate intravenously, and β2-agonist (e.g., nebulized or IV salbutamol).
125
What is the mechanism of action of calcium gluconate in the treatment of hyperkalemia?
Calcium gluconate works by membrane stabilization. It has a rapid effect on reducing hyperkalemia, but its action is transient.
126
What is the mechanism of action of insulin with dextrose in the treatment of hyperkalemia?
Insulin with dextrose drives potassium into cells. It has a rapid effect and intermediate action but may cause hypoglycemia.
127
What is the mechanism of action of sodium bicarbonate in the treatment of hyperkalemia?
Sodium bicarbonate transfers potassium into cells by exchange for hydrogen across the membrane. It has a rapid effect and intermediate action, and it is most effective in cases of metabolic acidosis. However, caution should be exercised to avoid sodium overload.
128
What is the mechanism of action of salbutamol in the treatment of hyperkalemia?
Salbutamol transfers potassium into cells. It has a rapid effect but short action. However, frequent use can raise serum lactate and may have side effects such as tachycardia and vasodilator effects.
129
What are the treatment options to reduce total body potassium if renal function is not improving after emergency treatment?
The treatment options to reduce total body potassium include renal replacement therapy (especially if combined with fluid overload) or ion exchange resin, such as calcium resonium, administered orally or rectally to bind potassium within the gut.
130
What should be done if pulmonary edema is suspected?
If pulmonary edema is suspected, a chest X-ray should be performed immediately (if safe to do so). The patient should be positioned upright, intravenous infusions should be stopped, high-flow oxygen should be administered, and oxygen saturations should be monitored with a target of achieving SaO2 greater than 94%.
131
What are the clinical manifestations of pulmonary edema?
Pulmonary edema presents as acute shortness of breath, anxiety, tachycardia, tachypnea, cool peripheries, and widespread crepitations/wheeze.
132
What are the treatment options for pulmonary edema?
Treatment options for pulmonary edema include intravenous diamorphine for vasodilatory and anxiolytic effects, intravenous GTN infusion if systolic BP is greater than 100mmHg, intravenous furosemide, regular review, and consideration of a higher level of support in the presence of specific signs and symptoms. CPAP can also be helpful in treating pulmonary edema.
133
What should be considered when making a nephrology referral?
When making a nephrology referral, the following factors should be considered: the clinical scenario and suspected diagnosis, the patient's premorbid state, the most recent creatinine, serum potassium, and ABG results, the patient's volume and cardiovascular status, the volumes of urine the patient is passing, the pre-insult renal function, the findings from ultrasonography, and the drugs the patient is taking, particularly nephrotoxic ones.
134
What is the prognosis for recovery in acute kidney injury (AKI)?
As individual nephrons recover, the kidney behaves similarly to chronic renal failure (CRF). However, because only a proportion of the nephron mass has recovered, each nephron has a higher solute load to excrete, limiting the kidney's ability to conserve sodium, potassium, bicarbonate, and water. With modern management, major problems with fluid and electrolyte losses are unusual, except in cases of postobstructive diuresis. The recovering kidney should not be exposed to further hypotensive or nephrotoxic insults. By 6 months, the kidney usually recovers 85-90% of premorbid function, but around 10% of patients may progress to CRF requiring permanent renal replacement therapy or transplantation. Prognosis is often determined by the severity of the underlying incident that caused the injury, with in-hospital AKI due to ATN carrying a 20-30% mortality rate, commonly due to infection or cardiovascular complications.
135
What are some future developments in the field of acute kidney injury (AKI)?
In the field of AKI, new "biomarkers" are being sought to identify and predict those at risk of impending AKI, as creatinine and urine output are relatively insensitive markers of renal function. Examples of these biomarkers include neutrophil gelatinase-associated lipocalin and kidney injury marker-1.
136
How is chronic kidney disease (CKD) defined?
CKD is defined as chronic irreversible loss of nephron mass resulting in permanent impairment of solute waste excretion.
137
What factors should be considered in the perioperative period for patients with subclinical stage 3 CKD?
Patients with subclinical stage 3 CKD (GFR 30-60ml/min) require special attention in the perioperative period due to the significant risk of developing AKI, multiple medications (especially cardiovascular drugs), concomitant silent cardiovascular disease, abnormal cardiovascular physiology, abnormal gastrointestinal function, and abnormal drug handling.
138
What precautions should be taken when depriving patients with CKD of oral fluid prior to surgery?
Depriving patients with CKD of oral fluid for extended periods of time, greater than 4-6 hours, should be avoided unless fluid is given intravenously.
139
Is preoperative transfusion necessary for patients with severe CKD?
Preoperative transfusion for patients with severe CKD is seldom necessary and can acutely impair renal function.
140
What are the five points to consider in the development of acute kidney injury (AKI)?
The five points to consider in the development of AKI are: 1) the kidneys cannot function without adequate perfusion, 2) renal perfusion is dependent on adequate blood pressure, 3) a surgical patient with poor urine output usually requires more fluid, 4) absolute anuria is usually due to urinary tract obstruction, and 5) poor urine output in a surgical patient is not initially treated with diuretics.
141
What are some potential complications that may arise after surgery, and why is it important to recognize any deterioration early?
Potential complications that may arise after surgery include infection, hemorrhage, ischemia, or incomplete resolution of the original pathology. It is important to recognize any deterioration early to intervene before the advent of organ failure.
142
Can you provide examples of anticipated postoperative complications associated with specific surgical presentations?
Yes, here are some examples: infarcted bowel from intestinal ischemia can lead to further ischemia causing anastomotic breakdown, abscess/collection, or fistula formation; ruptured abdominal aortic aneurysm can result in reactive or secondary hemorrhage/abdominal compartment syndrome/lower limb ischemia/postoperative ileus in open repair, or stent thrombosis and limb ischemia/abdominal compartment syndrome/renal impairment in endovascular repair; diverticular abscess and systemic sepsis can lead to anastomotic leak and recurrent sepsis or intraperitoneal abscess; penetrating abdominal trauma increases the risk of sepsis and may require laparostomy if regular relook laparotomy is needed; appendicitis can result in wound infection and abscess formation or intraperitoneal pelvic collection.
143
What is abdominal compartment syndrome (ACS)?
Abdominal compartment syndrome is the presence of elevated intra-abdominal pressure, which can cause significant morbidity and mortality among critically ill surgical and medical patients.
144
What is intra-abdominal hypertension (IAH)?
Intra-abdominal hypertension is a continuum of pathophysiological changes that begins with a disturbance of regional blood flow and can progress to abdominal compartment syndrome. It can be caused by intra-abdominal or extra-abdominal factors, such as trauma, pancreatitis, burns, or sepsis.
145
How is intra-abdominal pressure (IAP) measured?
Intra-abdominal pressure is measured in mmHg, with the usual level being subatmospheric to 0mmHg. Elevation to the range of 5–7mmHg is common.
146
What are the grades of intra-abdominal hypertension (IAH)?
IAH is graded based on the sustained or repeated elevation of IAP: Grade I (12–15mmHg), Grade II (16–20mmHg), Grade III (21–25mmHg), and Grade IV (>25mmHg). Grade IV requires surgical decompression.
147
What is the cardiac effect of abdominal compartment syndrome (ACS)?
ACS can cause elevation of the diaphragm and a subsequent rise in intrathoracic pressure, leading to reduced venous return and cardiac output. Hypotensive patients are at higher risk, and early signs of pressure elevation should be managed with fluid resuscitation.
148
What is the treatment for abdominal compartment syndrome (ACS)?
The treatment for ACS is to decompress the abdomen by re-opening or performing a laparotomy wound. Thorough washout, inspection for bleeding sites, and careful examination of the bowel for signs of ischemia should be performed. Various temporary abdominal closure devices, such as saline infusion bags or specific bowel bags, can be used. Close collaboration with ICU staff is important for postoperative management and achieving wound closure.
149
Why is aggressive fluid resuscitation important in the management of limb compartment syndrome?
Aggressive fluid resuscitation is required to minimize the effects of myoglobin release from muscle breakdown, which can cause acute kidney injury.
150
What can lead to lower limb compartment syndrome?
Lower limb trauma, associated hypotension, and prolonged operation in the lithotomy position can lead to a rise in interstitial pressure and subsequent compartment syndrome.
151
How can the diagnosis of compartment syndrome be confirmed?
If there is any doubt in the diagnosis, compartment pressures can be measured by inserting a needle into each compartment. Tissue necrosis can occur with an interstitial pressure as low as 30mmHg.
152
Which compartments of the leg require decompression in the management of compartment syndrome?
The lateral compartment, superficial posterior compartment, deep posterior compartment, and anterior compartment of the leg all require decompression.
153
What is burst abdomen?
Burst abdomen is a complication that occurs after surgery, characterized by wound dehiscence with exposure of the abdominal viscera.
154
How should burst abdomen be managed initially?
The immediate management of burst abdomen is similar to a laparostomy, with the goal of keeping the exposed viscera warm and moist and minimizing fluid and temperature loss.
155
What is the "pink fluid sign" associated with burst abdomen?
The "pink fluid sign" refers to the serosanguinous discharge that occurs around 8-10 days after the initial surgery, indicating the development of burst abdomen.
156
Under what conditions can the abdomen be resutured in burst abdomen cases?
If there is little systemic upset and the wound can be closed without tension, the abdomen may be resutured within 3-4 hours. However, if there is systemic instability, temporary management as a laparostomy is recommended.
157
What should be done if primary haemorrhage is difficult to control during surgery?
If primary haemorrhage is difficult to control, particularly from the liver, pelvis, or other inaccessible sites, packing the affected area can be considered. The patient should then be returned to the operating theatre at 48 hours for removal of the packs and reinspection of the operative site.
158
When does reactive haemorrhage occur and what should be done if it is suspected?
Reactive haemorrhage occurs in the immediate postoperative phase and may present while the patient is in recovery or after returning to the ward. A thorough systematic assessment should be conducted to promptly detect reactive haemorrhage, and if ongoing bleeding is suspected, more senior help should be sought early. Serial fluid challenges can be given to assess the patient's response and guide decision-making.
159
When does secondary haemorrhage typically occur and what may be required for control?
Secondary haemorrhage typically occurs 7-8 days following a procedure. It is often related to infective complications and can be unexpected. More proximal vascular control may be required and should be considered at the time of reoperation.
160
What is the recommended surgical treatment for necrotising fasciitis?
Prompt and aggressive debridement is the recommended surgical treatment for necrotising fasciitis. This involves wide excision of all involved tissue back to the bleeding edges. The debridement may be extensive and may require more than one operation. Patients also require systemic support on critical care, including broad-spectrum antibiotics and consideration of immunoglobulin therapy.
161
What are the initial features of necrotising fasciitis?
The initial features of necrotising fasciitis may include influenza-like symptoms, localized discomfort or pain, and swelling in the affected limb or area. A purplish rash may also be present. As the condition progresses, the skin may blister and release blackish fluid, and patients may experience severe systemic collapse due to sepsis.
162
What are the signs of anastomotic leakage?
The signs of anastomotic leakage include systemic instability, abdominal pain, rigid abdomen, tachycardia, and fever.
163
How may anastomotic leakage present in a more subtle manner?
Anastomotic leakage may present in a more subtle manner with low-grade fever, prolonged ileus, or failure to thrive.
164
Does the presence of a defunctioning stoma exclude the possibility of an anastomotic leak?
No, the presence of a defunctioning stoma does not exclude the possibility of an anastomotic leak.
165
What is the recommended management for major leakage?
Prompt reoperation is indicated for major leakage, with exteriorisation of suitable ends of the small and large bowel.
165
What is the recommended radiological procedure for diagnosing a leak?
CT with intravenous contrast is the radiological procedure of choice for diagnosing an anastomotic leak.
166
What are the challenges in managing intestinal fistulae?
The management of intestinal fistulae involves significant challenges and may require high-dependency care. It includes monitoring fluid and electrolyte losses, replacement, nutritional therapy, and physical management of the fistula.
167
What are the risk factors for intestinal anastomotic leakage?
Risk factors for intestinal anastomotic leakage include anastomotic technique, local factors such as obstruction, ischaemia, or peritonitis, and systemic factors such as shock, age, malnutrition, and immunosuppression.
168
What does the 'SNAPS' protocol stand for in assessing postoperative fistula?
The 'SNAPS' protocol stands for sepsis, nutrition, anatomy, procedure, and skin care. It is a protocol used to assess and manage postoperative fistulae.
169
What should be done to protect the surrounding skin in the management of a fistula?
The surrounding skin in the management of a fistula should be protected by dressings or bags, and the input of a stoma therapist may be required.
170
How long is usually the minimum time required for an adequate seal to form after the placement of a feeding stoma?
Ten days is usually the minimum time required for an adequate seal to form after the placement of a feeding stoma.
171
What are the different types of faecal stomas?
The different types of faecal stomas are temporary, loop, and end type.
172
What should be assessed when inspecting a stoma?
When inspecting a stoma, the assessment should include the colour/perfusion of the stoma, contents of the bag, skin around the stoma, and digital examination of the stoma.
173
What is the primary management objective in post-surgical wound management?
The primary management objective in post-surgical wound management is the prevention of surgical wound infections.
174
When should prophylactic antibiotics be used in post-surgical wound management?
Prophylactic antibiotics should be used in post-surgical wound management based on local policy and the perioperative risk and/or potential consequences of infection.
175
What should be the basis for empirical treatment while awaiting culture results in wound infections?
Empirical treatment while awaiting culture results should be based on the underlying procedure, not the site of the infection.
176
How does major but uncomplicated surgery affect fluid retention and urine output?
Major but uncomplicated surgery causes activation of antidiuretic hormone (ADH) and angiotensin-aldosterone, resulting in fluid retention and reduced urine output for 24-48 hours.
177
What information should be taken into consideration during clinical assessment?
Age, BMI, lean body mass, general condition, operative treatment and timing, comorbid diseases, and drugs should be taken into consideration during clinical assessment.
178
What is the daily water requirement for patients?
Patients usually need 1500-2000ml of water daily.
179
What is the basal water requirement?
The basal water requirement is 30-40ml/kg/day.
180
What are the normal basal requirements for sodium?
The normal basal requirements for sodium are 50-100mmol/day.
181
What are the possible management options for hyponatraemia?
The management of hyponatraemia may include sodium chloride infusion, water restriction, or diuretic plus water restriction depending on clinical assessment of volume status.
182
What is the usual requirement for potassium?
The usual requirement for potassium is 40-80mmol/day.
183
What are the common causes of hypokalaemia in surgical practice?
Common causes of hypokalaemia in surgical practice include renal losses, intestinal losses, and medical losses such as high nasogastric outputs.
184
What should be done to maintain the plasma potassium level above 3.5mmol/L?
To maintain the plasma potassium level above 3.5mmol/L, any avoidable losses should be stopped and potassium should be administered.
185
What are the consequences of a rapidly rising plasma potassium level?
Respiratory muscle weakness and cardiac arrest
186
What is the primary route of potassium excretion?
Via the kidney, in the distal nephron
187
What factors can impair the excretion of potassium?
Renal failure, hypoadrenalism, distal nephron disease, or drugs that affect the renin-aldosterone system
188
When are patients with impaired renal excretion particularly vulnerable to a sudden movement of potassium out of cells?
When there is trauma, drugs (suxamethonium), ischaemic/hypoxic damage, or a sudden rise in hydrogen ion concentration
189
What should be considered when measuring total calcium levels in the plasma?
The albumin level or directly measuring the ionised fraction
190
Give an example of a scenario where a patient with impaired renal excretion is vulnerable.
A hypovolaemic patient with metabolic acidosis, induced with suxamethonium, underventilated, and suffers a cardiac arrest
191
What is the active component of calcium in the plasma?
The ionised fraction
192
What conditions may cause apparent severe hypocalcaemia in critically ill patients?
Acute pancreatitis, acute rhabdomyolysis, and following thyroid or parathyroid surgery
193
How is hypocalcaemia treated?
Administration of calcium, treatment of the primary condition, and administration of activated vitamin D analogues in certain cases
194
When should calcium administration be limited in critically ill patients?
To cases with clinical evidence of hypocalcaemia or very low ionised calcium levels (usually <1mmol/L)
195
What are the symptoms and signs of hypocalcaemia?
Symptoms: tetany, numbness, paraesthesia
Signs: Chvostek's sign, Trousseau's sign, seizures
Signs: Chvostek's sign, Trousseau's sign, seizures
195
What are the consequences of severe hypercalcaemia?
Damage to neural tissue and renal tubular function
195
How does hypercalcaemia affect the kidney's function?
It diminishes the kidney's ability to retain salt, resulting in hypovolaemia and reduced calcium excretion
196
What are the possible causes of hypercalcaemia in critically ill patients?
Paraneoplastic hypercalcaemia, primary or secondary hyperparathyroidism
197
What are the symptoms of hypercalcaemia?
Malaise, abdominal pain, possible ureteric colic, dysrhythmias
198
What is the recommended treatment for hypercalcaemia?
Establishing a saline diuresis, administering a bisphosphonate intravenously, and treating the primary cause
199
What is the role of magnesium in the body?
Magnesium is essential for the normal functioning of nerve and muscle.
199
What are the consequences of magnesium depletion?
Confusion, seizures, and a range of dysrhythmias.
200
How should magnesium supplementation be done in the acute stage?
Intravenously to avoid the purgative effects of magnesium salts.
200
What causes hypomagnesaemia in critically ill patients?
Severe insults like peritonitis, chronic losses from the bowel or kidney, and alcohol abuse.
201
What is the recommended plasma level for magnesium?
It should not exceed 1.5mmol/L.
202
Why should magnesium levels be checked in critically ill patients with dysrhythmias?
Treatment with magnesium helps control dysrhythmic states.
202
What is the most common cause of hypermagnesaemia in critically ill patients?
Iatrogenic administration in the presence of impaired renal function.
203
How is phosphate absorbed in the body?
It is absorbed from the gut, especially from protein-containing food.
204
What influences the excretion of phosphate by the kidney?
Parathyroid hormone
204
What conditions can lead to high phosphate levels?
Renal impairment or massive muscle or bowel necrosis
205
What are the consequences of hypophosphataemia?
Effects on skeletal muscle function and the immune system
206
How is intravenous supplementation of phosphate given?
It needs to be given slowly over 24 hours when levels fall below 0.6mmol/L.
207
What are trace metals and their importance in the body?
Trace metals like zinc, copper, and selenium are essential for normal cellular function and the healing process.
208
When should measurement and supplementation of trace metals be considered?
In situations where there is prolonged dependence upon parenteral feeding or prolonged gut dysfunction.
209
What factors should be considered when prescribing fluid and electrolytes in critically ill patients?
Basal requirements, pre-existing fluid and electrolyte excess or deficit, and continuing abnormal losses.
210
What are the basal requirements for fluid and electrolytes in the body?
1500-2500ml of water, 100mmol of sodium, and 80mmol of potassium.
211
What type of fluid is required to maintain adequate extracellular volume?
Isotonic fluid for sodium
211
What is the priority when addressing abnormal losses of water with or without electrolytes?
Restoring plasma volume
211
How should intravenous fluids be used in the critically ill?
For as short a period as possible, particularly after uncomplicated elective surgery.
212
What are some examples of losses that consist mainly of extracellular fluid (ECF) or its equivalent?
Blood loss, vomiting, diarrhea, gut fistulae, unwell patients, diabetes mellitus
213
What are some examples of losses that are primarily water?
Fever, increased respiratory rate, prolonged water deprivation, diabetes insipidus
214
Why should the restoration of water deficit and electrolyte deficits be done gradually?
To avoid rapid shifts of water across membranes and potential complications like cerebral edema
215
What is a balanced salt solution used for in fluid replacement?
To replace extracellular fluid deficits (blood volume, interstitial volume)
216
What is the recommended timeframe to correct electrolyte deficits?
Over 48-72 hours
217
What are some examples of balanced salt solutions?
Normal saline (0.9% sodium chloride) and lactated Ringer's buffer (Hartmann's solution)
218
How much of the volume of a balanced salt solution remains in the vascular space?
About a third
219
Why is the redistribution of a balanced salt solution into the interstitial space usually desirable?
Because reduced intravascular volume is usually accompanied by an extracellular fluid deficit
220
What can happen with overprescription of normal saline?
Hyperchloraemia and acidosis
221
What electrolyte imbalance may be present if water only has been taken orally to compensate for fluid loss?
Hyponatraemia
222
What electrolyte is universally depleted with marked diarrhea?
Potassium
222
What happens to potassium during metabolic acidosis?
It moves from within cells to the extracellular compartment in exchange for extracellular hydrogen ions
223
What ions are lost from the stomach during vomiting or nasogastric drainage?
Hydrogen (H+) and chloride (Cl-) ions
224
What should be considered if blood results and patient clinical examination do not add up?
Measuring urine electrolytes and plasma osmolality
224
What can adequately replace the deficit caused by acid loss during vomiting or nasogastric drainage?
Normal saline, as endogenously produced acid (H+) will be retained by the kidney
225
What is the leading cause of mortality in surgical patients worldwide?
Sepsis
226
What are some signs and symptoms associated with sepsis?
Vasodilation, enhanced capillary leak, myocardial depression
227
Which mediators are involved in sepsis and have vasoactive properties?
Nitric oxide, bradykinin, histamine, prostaglandins, cytokines
228
Which cytokines are involved in sepsis and contribute to the pyrexia and hypermetabolic state?
Interleukin 1 (IL-1), tumor necrosis factor, IL-6
228
What is the potential consequence of excessive and unregulated activation of mediator pathways in sepsis?
Development of multiple organ dysfunction (MODs)
229
What is the definition of sepsis according to the Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3)?
Life-threatening organ dysfunction caused by a dysregulated host response to infection
230
How is septic shock defined?
A condition characterized by profound circulatory, cellular, and metabolic abnormalities associated with a greater risk of mortality than sepsis alone
231
What methodology is used to determine organ dysfunction in sepsis?
Sequential Organ Failure Assessment (SOFA)
231
How is septic shock clinically recognized?
Response to treatment: persistent hypotension after fluid resuscitation, persistent lactate above 2mmol/L, vasopressor requirement to maintain MAP ≥65mmHg in the absence of hypovolemia
232
What is the first step in screening and managing infection according to the Surviving Sepsis Campaign (SSC)?
Identification of infection
232
What are the criteria for organ dysfunction according to qSOFA?
Respiratory rate over 22, systolic blood pressure less than 100mmHg, altered mentation (each scores 1 point)
232
What is the modified version of SOFA used for early detection of sepsis?
Quick SOFA (qSOFA)
233
Why is it difficult to definitively diagnose septic shock in a ward setting?
Invasive monitoring is necessary to rule out hypovolemia
234
What should be done in patients identified as having infection according to the SSC?
Obtain blood and other cultures, administer tailored antibiotics, and evaluate for infection-related organ dysfunction
235
How should patients with sepsis be identified according to the SSC?
By the organ dysfunction criteria, including lactate level above 2mmol/L
236
What can be used as a secondary screen to identify patients at risk for clinical deterioration according to the SSC?
Evidence of two out of three qSOFA elements in patients who have screened positive for infection
237
What should be implemented in patients with infection and hypotension or a lactate level greater than or equal to 4mmol/L according to the SSC?
Providing 30ml/kg crystalloid with reassessment of volume responsiveness or tissue perfusion
238
What should be done if organ dysfunction is identified in patients with sepsis according to the SSC?
Ensure that step 1 elements have been initiated, such as obtaining blood cultures and administering broad-spectrum antibiotics
239
What is the purpose of qSOFA in identifying patients at risk of sepsis according to Sepsis-3?
To identify patients with a higher risk of hospital death or prolonged ICU stay
240
Does qSOFA define sepsis?
No, but the presence of two qSOFA criteria predicts increased mortality and ICU stays of more than 3 days in non-ICU patients
241
What concept has the Surviving Sepsis Campaign recommended to aid sepsis management?
Care bundles
242
What are the two recommended management packages or 'care bundles' according to the SSC?
The 3-hour care bundle and the 6-hour care bundle
243
What is the goal of the 3-hour care bundle?
To optimize the care of patients with sepsis within the first 3 hours after presentation
243
What are the 'Sepsis Six'?
Six tasks easily performed by non-specialist staff that form the crucial first steps in delivering the care bundle: high-flow oxygen, blood cultures, intravenous antibiotics, intravenous fluid resuscitation, haemoglobin and lactate level check, accurate hourly urine output measurement
243
What additional elements are included in the 3-hour care bundle?
Ensuring broad-spectrum antibiotics have been given and administering 30ml/kg crystalloid for hypotension or lactate ≥4mmol/L
244
What should be done for patients with persistent hypotension or increased lactate according to the SSC?
Managed with early goal-directed therapy (EGDT)
244
What is recommended in the 6-hour care bundle for maintaining MAP in patients with hypotension?
Apply vasopressors to maintain a MAP ≥65mmHg
245
What should be done in the event of persistent hypotension or elevated lactate according to the 6-hour care bundle?
Reassess volume status and tissue perfusion, document findings, and remeasure lactate if initial lactate is elevated
246
What can help achieve source identification and control quickly in sepsis management?
The CCrISP three-stage assessment process
247
What is the mortality risk when three or more organ systems have failed?
Approaches 80-100%
248
What are some supportive measures that can be taken to manage multiple organ dysfunction?
Ventilation, hemofiltration/hemodialysis, inotropic support, nutritional support, use of blood products
249
What is ARDS and how does it develop?
ARDS is adult respiratory distress syndrome, a diffuse inflammatory process often associated with sepsis. It is characterized by 'waterlogged' lungs due to extravasation of inflammatory fluid and cells
250
What is the recommended treatment for ARDS?
Respiratory support, usually mechanical ventilation, and early involvement of expert critical care
251
What are the main factors contributing to cardiovascular failure in sepsis?
Loss of peripheral vascular tone (vasodilatation), loss of circulating volume (hypovolemia), and myocardial depression (pump failure)
252
Why is renal dysfunction common in sepsis?
Due to acute kidney injury, often established during the early stages of sepsis, and compounded by circulating nephrotoxins
252
What is the recommended treatment for cardiovascular failure in sepsis?
Close monitoring of cardiovascular status, fluid resuscitation, and inotropic and vasopressor support if needed
253
What signs should be actively excluded as potential indicators of sepsis?
Tachycardia, tachypnea, raised WBC, hyper- or hypothermia
254
What are some other conditions that can cause an inflammatory response similar to sepsis?
Pancreatitis, ischemia, multiple trauma, and hemorrhagic shock
255
What are some causes that may lead to organ dysfunction in surgical patients?
Can include causes from different boxes depending on the stage, such as ischaemic gut, pancreatitis, ischemia, multiple trauma, and hemorrhagic shock
255
What can worsen the prognosis if not promptly accomplished in the management of patients with signs of organ dysfunction?
Failure to accomplish any of the essential points of management
256
What should be assessed during a full patient assessment in a case of suspected sepsis?
Vital signs, capillary refill time, urine output, lactate level, history, and systematic examination
256
What are the immediate steps to be taken in the assessment and management of a patient with suspected sepsis?
Treatment with high-flow oxygen via a facemask, establishment of IV access with volume expansion, and rapid volume expansion with crystalloid
257
What are some common causes of postoperative fever or sepsis in recovering surgical patients?
Chest infection, anastomotic leak, central venous line infection
258
When do central line infections become more frequent?
In lines more than 48 hours old or those being used for TPN
258
When does anastomotic leak typically occur in postoperative patients?
From day 4 onwards
258
When may liver enzymes be abnormal in sepsis?
When the biliary tree is the primary source of sepsis or as part of multiorgan dysfunction
259
What should be checked in the white blood cell count in cases of sepsis?
Abnormally high (>10×109/L) or low (<2×109/L) counts
260
What imaging techniques can be used to evaluate possible sites of sepsis?
Ultrasound, CT, laparotomy
260
What may ABG analysis show in cases of sepsis?
Hypoxaemia, metabolic acidosis, and raised lactate levels
261
What investigations may be required for immunocompromised patients with sepsis?
Specific investigations such as bronchoalveolar lavage or induced sputum sampling
261
What type of fluid replacement is usually appropriate in cases of sepsis?
Crystalloids
262
What is the recommended treatment for an infected prosthesis?
Removal of the prosthesis and long-term antibiotics
263
What should be considered in patients with prostheses and MRSA infection?
A very high mortality risk and the need for removal of the prosthesis
263
What should be carefully balanced before giving antibiotics for a positive culture in ICU patients?
Presence of a host response, site of potential infection, and the need to avoid superinfection or antibiotic resistance
264
What measures should be taken perioperatively to prevent complications?
Give prophylactic antibiotics, perform surgery rapidly, cleanly, and haemostatically, and electively perform operations whenever possible
264
What are the criteria for defining malnutrition according to NICE?
BMI <18 kg/m2, unintentional weight loss >10% within the last 3–6 months, or BMI <20 kg/m2 and unintentional weight loss >5% within the last 3–6 months
265
What percentage of surgical patients have malnutrition upon admission to the hospital?
Up to 60%
265
Why may people admitted in a good nutritional state develop malnutrition as inpatients?
Due to surgical pathology, metabolic response to illness, or inadequate oral intake while in the hospital
265
What are the risk factors for developing malnutrition in the hospital?
Poor oral intake for more than 5 days, poor absorptive capacity, high nutrient losses, increased nutritional needs from causes such as catabolism
266
What metabolic changes occur with starvation?
Fall in insulin levels, rise in glucagon levels, depletion of hepatic glycogen stores, adaptation to use fatty acids as the main fuel source, preservation of protein where possible, and reduced metabolic rate
267
What happens to the body's metabolism during fasting?
Insulin levels fall, glucagon levels rise, hepatic glycogen stores deplete, and the body adapts to use fatty acids as the main fuel source
268
What happens to fatty acids during fasting?
They undergo beta-oxidation to form acetyl-coA, which can be converted to ketone bodies in the absence of sufficient oxaloacetate
269
What is the impact of continued starvation on protein loss and ketone body production?
Protein losses eventually decrease to around 20g/day, and the liver increases its capacity for ketone body production
270
What are the effects of sympathetic nervous system stimulation during the stress response?
Release of adrenal catecholamines, leading to tachycardia and vasoconstriction
270
What is activated during the stress response to promote sodium and water retention?
The renin-angiotensin-aldosterone system
271
What hormone is released in response to increased levels of adrenocorticotrophic hormone (ACTH) during the stress response?
Glucocorticoids, including cortisol
271
Why is hyperglycemia common during the stress response?
Due to impaired peripheral glucose uptake and inhibition of insulin release
272
What is the recommended blood glucose target for critically ill patients during the stress response?
8-10mmol/L
273
What is the primary energy substrate once glucose cannot be effectively used during the stress response?
Fatty acids released via lipolysis
274
What happens to insulin resistance and metabolic state as the stress response subsides?
Insulin resistance falls, and there is a shift towards net anabolism
275
What happens to insulin resistance and fuel reliance in septic patients?
Insulin resistance develops, and there is a greater reliance on fat as fuel
276
What can contribute to the exaggerated muscle protein breakdown in sepsis?
Hormonal environment and the release of cytokines such as IL-1, IL-6, and tumor necrosis factor (TNF)
276
When should nutritional screening be conducted for hospitalised patients?
On admission and at least weekly thereafter during their inpatient stay
277
What is the most commonly used nutritional screening tool in the UK?
MUST (Malnutrition Universal Screening Tool)
278
What information can be gathered from a patient's history and examination regarding nutritional status?
Weight loss, altered/poor nutritional intake, increased gastrointestinal losses, and non-specific examination findings such as cachexia, edema, skin changes, and muscle wasting
279
What are some anthropometric measures used to assess nutritional status?
BMI, skinfold thickness measurements, mid-arm circumference (MAC), and mid-arm muscle circumference (MAMC)
279
What factors can contribute to reduced muscle strength in critical illness?
Impaired consciousness, critical illness polyneuropathy/myopathy, and edema
279
What can MAC and MAMC be used to estimate?
Fat/muscle ratios
280
What is the significance of albumin in assessing nutritional status?
In the wider population, it is used as a marker of protein deficiency in chronic malnutrition
281
What can a renal profile help assess in acutely unwell patients?
Hydration status
281
Why are equations for calculating energy expenditure often inaccurate in critically ill patients?
They can result in under- or over-feeding
282
What are the options available for providing nutritional support to patients at risk of malnutrition?
Enteral nutrition (supplementation of oral intake, nasogastric feeding, nasojejunal or nasoduodenal feeding, tube enterostomy) and parenteral nutrition
283
When should enteral feeding be maintained?
When possible and in compliant patients who have no swallowing problems and are still maintaining some oral intake
284
What are the absolute contraindications to nasogastric feeding?
Mechanical bowel obstruction, suspicion of ischaemic bowel, massive gastrointestinal hemorrhage, or patient refusal (if the patient has capacity)
285
What are the relative contraindications to nasogastric feeding?
Severe diarrhea/vomiting, circulatory shock states, proximal small bowel fistula, conditions where nasogastric tube placement may be unsafe (e.g., major maxillofacial surgery, skull base fracture, or esophageal varices)
285
What is important during nasogastric feeding in critically ill patients?
Maintenance of 30-45° head-up positioning to reduce the risk of aspiration
286
What are prokinetics and how are they used in the treatment of gastroparesis?
Prokinetics are drugs that increase luminal transport and strengthen smooth muscle contraction in the gut. Commonly used drugs include metoclopramide, erythromycin, and domperidone
287
What alternative feeding methods may be considered if high aspirates continue despite treatment for gastroparesis?
Post-pyloric feeding or parenteral nutrition
288
Why is intraoperative insertion of a nasogastric tube considered in surgical patients?
To provide postoperative nutritional support while the patient is still under general anesthesia
289
What safety concern was raised by the National Patient Safety Agency (NPSA) regarding nasogastric tube feeding?
Injuries/deaths occurring in patients fed via misplaced NGTs
290
What is the criteria for confirming the correct positioning of a nasogastric tube?
pH testing (pH between 1 and 5.5) or X-ray confirmation
291
How often should pH testing be done in patients receiving nasogastric feed?
At least once daily and prior to feeding or administering medication
292
What can be used to prevent patients from pulling out their nasogastric tubes?
A bridle device, which uses catheter-mounted magnets and tape to secure the tube and make it more difficult to remove
292
What methods are used for the insertion of post-pyloric feeding tubes?
Bedside insertion (with radiological confirmation), direct vision during surgery, endoscopic placement, and fluoroscopically guided insertion
293
In which patients is post-pyloric feeding appropriate?
Patients in whom the nasogastric route is contraindicated, such as those with gastroparesis or postoperative patients with upper gastrointestinal tract anastomoses
294
What should be monitored in patients with post-pyloric tubes?
Signs of abdominal distension or vomiting, which may suggest outward tube migration, and the presence of feed in the gastric aspirate, which may suggest misplacement
294
When should tube enterostomy be considered?
In patients expected to require prolonged nutritional support (>4 weeks) or when oral/nasal access is not feasible in the short term
295
What are some absolute contraindications to tube enterostomy?
Uncorrected coagulopathy, distal mechanical bowel obstruction, and peritonitis/infection over the insertion site
296
What is the most commonly used method for tube enterostomy in postoperative/non-surgical patients?
Percutaneous endoscopic gastrostomy (PEG) using local anaesthetic infiltration and endoscopic guidance
297
When can feeding be initiated after uncomplicated PEG tube insertion?
4 hours after insertion
297
What types of feeding regimens are possible with enterostomy tubes?
Bolus or continuous feeds
298
What is tracheo-esophageal fistula, and when can it develop?
Tracheo-esophageal fistula is a connection between the trachea and esophagus. It can develop in patients with both endotracheal and nasoenteric tubes
299
What is a common complication of enteral feeding related to tube placement?
Tube displacement
299
What can be done to reduce the risk of aspiration during feeding?
Maintaining a head-up positioning, using proton pump inhibitors or H2-receptor antagonists, and considering prokinetics if delayed emptying is suspected
300
What is a common complication of enteral feeding that can occur in critically ill patients?
Diarrhea
301
What is a major source of hospital-acquired bacteraemia and mortality in patients receiving parenteral nutrition?
Catheter-related bloodstream infection (CRBSI)
301
What are some potential causes of diarrhea in critically ill patients receiving enteral feed?
Concomitant antibiotic administration, villous atrophy from prolonged periods without enteral nutrition, and gastrointestinal infections (e.g., Clostridium difficile)
302
How can the risk of CRBSI be reduced in patients receiving parenteral nutrition?
By adopting strict aseptic techniques during catheter insertion and handling, using antimicrobial-impregnated catheters, and allocating a dedicated lumen for TPN administration
303
Is pancreatitis a contraindication to TPN?
No, pancreatitis is not a contraindication to TPN
303
What is a potential complication when discontinuing parenteral nutrition?
Hypoglycemia
304
What is refeeding syndrome?
Refeeding syndrome occurs when carbohydrates are reintroduced rapidly to malnourished patients, leading to marked hypophosphatemia and potentially fatal consequences if not recognized.
304
What is "pre-emptive" analgesia?
It is a method where analgesic medications are administered or local anesthetic procedures are performed before the surgical trauma occurs. This proactive approach to pain management may have short and long-term advantages.
304
What happens to intracellular mineral stores during starvation/malnutrition?
During starvation/malnutrition, intracellular mineral stores become severely depleted over time, while serum levels remain relatively well preserved.
305
Is there a diagnostic test for refeeding syndrome?
No, there is no specific diagnostic test for refeeding syndrome. Diagnosis and treatment should be based on a suggestive history or clinical presentation.
306
Which minerals and vitamins are required for these processes?
Minerals such as phosphate, magnesium, calcium, and potassium, as well as vitamins like thiamine (essential cofactor in carbohydrate metabolism), are required for these processes.
307
How can poorly managed pain affect pulmonary function?
Poorly managed pain can further impair pulmonary function by restricting respiratory excursion, impairing the ability to cough and clear secretions, and predisposing to chest infections.
308
Why is bowel preparation no longer considered necessary in the preoperative phase?
Bowel preparation, which involves purgation with powerful laxatives, leads to dehydration, electrolyte imbalance, and prolongation of the preoperative starvation period. It is now considered unnecessary.
309
How does preoperative oral carbohydrate loading benefit patients?
Preoperative oral carbohydrate loading with a glucose solution allows patients to enter surgery in a "fed state," reducing the stress response to surgery by decreasing insulin resistance and catabolism.
309
What are the key treatment goals for refeeding syndrome?
The key treatment goals for refeeding syndrome include correcting mineral and vitamin deficits, initiating feeding under dietetic guidance, and closely monitoring for the development of clinical features and managing them appropriately.
310
What measures promote recovery in the postoperative period?
Recovery in the postoperative period is promoted by avoiding opiates and using paracetamol and non-steroidal anti-inflammatory drugs (NSAIDs) for gut function restoration, early commencement of postoperative diet, early and structured postoperative mobilization, early catheter removal, and administration of restricted amounts of intravenous fluid.
311
What is the recommended time for preoperative fasting?
Traditional wisdom suggested a considerable period of nil by mouth before surgery. However, it is now accepted that the last intake of food can be up to 6 hours before surgery, and clear fluids can be consumed up to 2 hours prior to surgery.
312
Why is it important to treat acute pain?
Control of pain is important not only for humanitarian reasons but also because uncontrolled pain can have negative effects on body physiology, which can affect the outcome of surgery. Uncontrolled pain can lead to sympathetic stimulation, increased heart rate, peripheral vascular resistance, visceral vasoconstriction, increased cardiac workload, myocardial ischemia, reduced blood flow to vital organs, restricted mobility, increased risk of developing deep vein thrombosis (DVT), and other complications.
313
What is the three-stage assessment process when called for postoperative analgesia problems?
The three-stage assessment process involves understanding the patient's physiological status and details of the surgery and interventions they have undergone. This includes reviewing the anaesthetic chart, drug prescription chart, and clinical notes, as well as discussing with the ward nursing staff and examining the patient.
314
What is the Numerical Rating Scale (NRS) used for?
Self-reporting of pain on an 11-point scale
315
What is the Visual Analogue Score (VAS) used for?
Patients indicate the intensity of their pain on a 100-mm horizontal line
316
What are the different groups of medications used for pain management?
Paracetamol, NSAIDs, opioids, and co-analgesics
316
What are the recommended dosages for paracetamol?
1g, 4- to 6-hourly up to a maximum of 4g in 24 hours
317
How is pain categorized on the NRS?
From no pain (0) to disabling severe pain (7-10)
318
What are the three steps of the World Health Organization analgesic ladder?
Step 1: simple analgesics, Step 2: weak opioids with or without simple analgesics, Step 3: stronger opioids with or without simple analgesics
319
What is the mechanism of action of NSAIDs?
Inhibition of prostaglandin synthesis by inhibiting the enzyme cyclooxygenase
320
What are some examples of NSAIDs?
Ibuprofen, diclofenac, ketorolac, naproxen
320
What are opioids derived from?
Opium alkaloids
321
How do opioids exert their analgesic effects?
By acting on mu-opioid receptors
322
What are some examples of weak opioids?
Codeine
322
What are some common side-effects of opioids?
Nausea and vomiting, constipation, itching, bladder retention, drowsiness, and respiratory depression
323
What is patient-controlled analgesia (PCA)?
A method that allows patients to control their pain by self-administering intravenous opioids in small boluses
323
What are some examples of strong opioids?
Morphine
324
What is the advantage of using PCA?
Patients can adjust the dose of opioids to achieve their desired level of pain relief
324
How does PCA maintain a constant plasma level of analgesic?
By allowing patients to make requests for medication through a hand-held device
325
What is the typical regimen for PCA with morphine?
1-2 mg boluses with a lockout interval of 5 minutes
325
What is the potency of oxycodone compared to morphine?
Twice as potent
326
What is an important side effect of codeine?
Constipation
326
What should be considered when prescribing codeine for elderly patients?
Regular laxatives may be prescribed to prevent constipation
327
What are some examples of co-analgesics?
Anticonvulsants (e.g., gabapentin), antidepressants (e.g., amitriptyline), and ketamine
327
What should be administered as a safety measure in patients receiving opioids?
Additional oxygen
328
What are regional analgesic techniques?
Techniques that involve the deposition of local anesthetics along the pain pathway to block neural structures and interrupt pain impulses
328
What are the categories of regional analgesic techniques based on the level of neural blockade?
Neuraxial (intrathecal, epidural), paraxial (thoracic paravertebral block), peripheral (brachial plexus nerve block, transversus abdominis plane block), and local (wound infiltration, periarticular infiltration after joint surgeries)
329
What is the typical combination used in epidural analgesia?
A combination of local anesthetic and opioids (e.g., bupivacaine 0.1% + fentanyl 2 μg/ml)
329
What is the mechanism of action of local anesthetics in regional analgesic techniques?
They inhibit sodium channels in neurons, preventing transmission along the nerves
330
What are the complications associated with regional analgesic techniques?
Damage to nerve roots or spinal cord, accidental dural puncture, hematoma formation, infection risks, sensory/motor blockade, hypotension, nausea, vomiting, pruritus, bladder retention, respiratory depression
330
What are the levels of the Bromage score and their corresponding motor functions?
0 = full flexion of knees and feet, 1 = just able to move knees, 2 = able to move feet only, 3 = unable to move feet or knees
331
How is hypotension managed in patients with a functioning epidural?
With a combination of intravenous fluids and vasopressors such as metaraminol infusions
332
What should be considered when managing hypotension in patients with a functioning epidural?
Fluid overload and excessive vasoconstriction should be avoided, and other causes of hypotension should be evaluated
