17- Trouma & ER Refrence 2 Flashcards
What are the signs of decreased tissue perfusion that can indicate shock?
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.
What are some common causes of cardiogenic shock in surgical patients?
Myocardial infarction, acute arrhythmias, post-cardiac surgery myocardial ‘stunning,’ and cardiac contusions due to trauma
What are the clinical features of cardiogenic shock?
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
How can cardiogenic shock be diagnosed in a surgical patient?
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
What are some clinical features of sepsis in the early stage?
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
What are the principal causes of obstructive shock?
Cardiac tamponade, tension pneumothorax, and pulmonary embolism
What are the specific features of obstructive shock?
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
What are the specific features of septic shock?
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.
What is the essential aim of treatment for sepsis?
Restoration of adequate perfusion at the cellular level
What are some clinical features of sepsis in the late stage?
Decreased level of consciousness, tachypnea, tachycardia, low cardiac output, systolic blood pressure less than 80mmHg, oliguria, metabolic acidosis, elevated blood lactate, cold extremities
What are the mainstays of early treatment for sepsis?
Infusion of fluid and administration of oxygen to improve cardiac output and oxygen transport
How should patients with shock be initially treated if cardiogenic and obstructive forms of shock are not suspected?
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
What is the recommended size for a peripheral cannula for venous access?
At least one large-bore (16G) peripheral cannula
Where is reliable venous access usually obtained from?
The antecubital fossa or via the cephalic vein at the wrist
What can be done if vasoconstriction makes it difficult to obtain venous access?
A “cut-down” procedure can be performed in the antecubital fossa or on the long saphenous vein in front of the medial malleolus
What should be done in profoundly shocked patients who cannot obtain initial access through peripheral veins?
Cannulate the femoral vein percutaneously in the groin
What urgent tests should be conducted when obtaining venous access?
Cross-matching, haematology, and biochemistry tests
Under what circumstances is a suprapubic catheter inserted?
When there is a possibility of urethral injury (as in severe pelvic fractures) or when dealing with young children
How is a suprapubic catheter inserted?
Under ultrasound control once the bladder has filled
How often should urine output be measured after bladder catheterization?
Hourly
Where is a pulse oximeter typically attached?
To a finger or ear lobe
How is a central venous catheter inserted?
Percutaneously via the internal jugular or subclavian veins
What does a low or negative CVP indicate in a shocked patient?
The need for more fluid
What does a very high CVP indicate in a shocked patient?
Right ventricular or biventricular failure and the need for diuretics, vasodilators, or inotropic agents, or an obstructive cause
What is the initial fluid management for shock?
Boluses of warmed crystalloid (up to 20 ml/kg body weight)
What influences the choice of fluid for initial replacement in shock?
The type of fluid lost
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)
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
What samples should be sent for bacteriological examination when sepsis is suspected?
Appropriate samples such as blood, urine, sputum, and drain fluids
Which are the most commonly used crystalloids for fluid resuscitation in shock?
Normal saline and Ringer’s lactate solution
Why is Ringer’s lactate preferred over normal saline for fluid resuscitation?
It can buffer metabolic acidosis and avoid hyperchloraemic acidosis
What is the theoretical risk of using Ringer’s lactate in patients with acute kidney injury or chronic kidney disease?
Hyperkalaemia
What is the theoretical advantage of colloid infusions over crystalloids?
They are retained more in the intravascular space
Do studies show any benefit of colloid use over crystalloid use in clinical outcomes?
No, there is no significant benefit
What are the risks associated with colloid infusions?
Anaphylaxis, coagulopathy, and acute kidney injury
What are the potential effects of crystalloid resuscitation compared to colloid resuscitation?
Greater weight gain and tissue edema with crystalloid use
How much crystalloid is required to replace a given amount of blood loss compared to colloid?
Approximately three times the volume
Is there a fixed relationship between serum albumin concentration and colloid osmotic pressure?
No, except when serum albumin falls very low
Do both colloids and crystalloids pass through the vascular basement membrane in septic shock with increased capillary permeability?
Yes
What is the recommended volume limit of crystalloid used during resuscitation?
<50% of non-blood fluid infusion
What is one of the most important steps in managing shocked patients?
Assessing the response to treatment
How often should the patient’s progress be reassessed during resuscitation?
At least every 30 minutes or so
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
What are the steps in the algorithm of cardiovascular monitoring/support?
- Establish and maintain normovolaemia; 2. Assess response; 3. CVP assessment; 4. Invasive monitoring and inotropic treatment
What are some signs that surgical patients may present with in cardiovascular compromise?
Oliguria, hypotension, tachycardia, hypoxia, acidosis
What are the indicators of inadequate CVP?
CVP <8cmH2O
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
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
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
What are the essential metabolic monitoring parameters in refractory shock?
Urea and electrolyte levels, arterial pH, blood gas measurements, blood lactate levels
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
What does the disappearance of metabolic acidosis indicate in the context of shock?
Adequate resuscitation and improved cardiac output
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
What does respiratory acidosis with an increase in arterial PaCO2 indicate?
The need for endotracheal intubation and assisted ventilation
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
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
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
What are some parameters that can be monitored in the cardiovascular system?
Blood pressure, CVP (central venous pressure), cardiac output or cardiac index (CI)
What is the priority in treating shock?
Restoring perfusion as a matter of urgency
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
What components of cardiac output can be monitored and manipulated?
Preload, cardiac function and compliance, afterload
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
What are the commonly used anatomical sites for arterial pressure monitoring?
Radial artery (most frequent), dorsalis pedis artery
What can the shape of the arterial waveform indicate in normal and pathological conditions?
Systemic vascular resistance and cardiac contractility
What are the potential contraindications for cannulating the radial artery?
Local sepsis and coagulopathy
What components are connected to the arterial cannula for pressure monitoring?
Short length of rigid tubing, three-way tap, flush device, and transducer
What factors influence central venous pressure (CVP)?
Venous return, right heart compliance, intrathoracic pressure, and patient position
What are some complications associated with arterial cannulation?
Haematoma, thrombosis, distal ischemia, intimal damage, false aneurysm formation, disconnection, injection of irritant drugs
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
How is the infraclavicular subclavian route typically performed?
Using ultrasound guidance for increased accuracy
Where should the catheter be advanced to?
A previously measured point so that the tip lies in the distal superior vena cava (SVC)
In which direction should the needle be advanced when performing the infraclavicular subclavian route?
Horizontally towards the suprasternal notch in a linear fashion
What should be done if the initial attempt is unsuccessful?
Systematically search with further straight insertions to locate the vein
Where should the cannula be inserted for this technique?
1-2cm below the midpoint of the clavicle
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
How should the artery be displaced during the ultrasound-guided approach?
Medially
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
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
When is ultrasound still recommended for emergency cases involving the subclavian route?
When poor visualization of the subclavian vein occurs behind the clavicle
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
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
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
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
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)
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
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
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
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
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
What information can be obtained from the waveform displayed by TOD?
Information on preload, stroke volume, and afterload
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
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
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
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.
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.
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.
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.
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.
Which drugs are commonly used as inotropes?
The most commonly used inotropes are adrenaline and dobutamine.
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.
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.
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.
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.
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.
What should the surgical team be aware of when treating AKI?
The life-threatening complications of AKI, such as hyperkalemia and pulmonary edema
What is one of the most common reasons why a surgical team may be called to see a patient?
Poor urine output
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
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
What is the current classification system for AKI?
The Acute Kidney Injury Network (AKIN) classification system
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
What are the three main categories of AKI etiology?
Prerenal, intrinsic renal, and post-renal
Which is the most common etiology of AKI in surgical patients?
Prerenal failure
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
What is the cause of post-renal failure?
Obstruction and back-pressure in the urinary tract
What are the urine output criteria for Stage 2 AKI?
Urine output of <0.5 ml/kg/h over 12 hours
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
What are the urine output criteria for Stage 1 AKI?
Urine output of <0.5 ml/kg/h over 6 hours
What are the GFR criteria for Stage 2 AKI?
An increase in creatinine of 2- to 3-fold from baseline
What are the GFR criteria for Stage 3 AKI?
An increase in creatinine of 3-fold from baseline or serum creatinine >354μmol/L
What are the urine output criteria for Stage 3 AKI?
Urine output of <0.3 ml/kg/h over 24 hours
What are the common causes of prerenal AKI?
Hypovolemia, sepsis, and low cardiac output
What are the common causes of intrinsic renal AKI?
Acute tubular necrosis, ischaemic injury, nephrotoxic injury, abdominal compartment syndrome, and hepatorenal syndrome
What are the common causes of post-renal AKI?
Bladder outflow obstruction and bilateral ureteric obstruction
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
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
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
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
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
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
What should be done if a patient with AKI presents with complete anuria?
Exclude urinary tract obstruction until proven otherwise
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
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
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
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
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
What should be done to exclude post-renal obstruction in AKI patients?
Perform ultrasonography to exclude post-renal obstruction and treat accordingly
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
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
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.
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.
When is renal replacement therapy (RRT) indicated in AKI management?
RRT is indicated when acute kidney injury fails to respond to other measures.
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.
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.
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.
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
What are the relative indications for initiating renal replacement therapy (RRT) in cases of AKI?
Acidosis (pH <7.2), uraemia, pericarditis, and toxin removal
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).
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.
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.
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.
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.
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.
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%.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
