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Submitted by Dr Shijo Dany Kurian
1st yr PG
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Postoperative complications may either be general or specific to the type of surgery undertaken and should be managed with the patient's history in mind.
Common general postoperative complications include postoperative fever, atelectasis, wound infection, embolism and deep vein thrombosis (DVT).
Specific complications occur in the following patterns: early postoperative, several days after the operation, throughout the postoperative period and in the late postoperative period
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IMMEDIATE Primary haemorrhage: either starting during
surgery or following postoperative increase in blood pressure - replace blood loss and may
require return to theatre to re-explore the wound.
Basal atelectasis: minor lung collapse. Shock: blood loss, acute myocardial infarction,
pulmonary embolism or septicaemia. Low urine output: inadequate fluid replacement
intra-operatively and postoperatively.
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Acute confusion: exclude dehydration and sepsis. Nausea and vomiting: analgesia or anaesthetic-
related; paralytic ileus. Fever Secondary haemorrhage: often as a result of
infection. Pneumonia. Wound or anastomosis dehiscence. DVT. Acute urinary retention. Urinary tract infection (UTI). Postoperative wound infection. Bowel obstruction due to fibrinous adhesions. Paralytic Ileus.
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Bowel obstruction due to fibrous adhesions. Incisional hernia. Persistent sinus. Recurrence of reason for surgery - eg,
malignancy.
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The following criteria must be fulfilled before a patient can be discharged from the recovery room
The patient is fully conscious, responding to voice or light touch, able to maintain a clear airway and has a normal cough reflex
Respiration and oxygen saturation are satisfactory (10-20 breaths per minute and SpO2 > 92%
The cardiovascular system is stable with no unexplained cardiac irregularity or persistent bleeding.
The patient’s pulse and blood pressure should approximate to normal preoperative values or should be at a level commensurate with the planned postoperative care
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pain and emesis should be controlled and suitable analgesic and anti-emetic regimens should be prescribed
temperature should be within acceptable limits (>36°C)
oxygen and fluid therapy should be prescribed when required.
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The first postoperative assessment should take place immediately after surgery on return to the ward.
It provides a baseline against which the patient’s condition may subsequently be assessed and identifies any problems that may have occurred on transfer from the operating department.
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The first postoperative assessment should determine:
intraoperative history and postoperative instructions
circulatory volume status respiratory status mental status.
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The following postoperative treatment and prophylaxis options should be discussed preoperatively :
adequate pain control venous thromboembolism prophylaxis antibiotic prophylaxis continuation of current medications substitution of current medication (eg
diabetic control, steroid therapy)
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Prophylaxis for postoperative nausea and vomiting
Ability of patients to take drugs by mouth Pressure area management.Postoperatively, consider the need for: physiotherapy nutrition team consultation oral hygiene.
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Surgical patients are usually seen once or twice a day on the ward round and their status must be documented.
Clear clinical notes must be kept and an entry made every time a patient is reviewed.
This assessment is the most complete opportunity to ensure that the patient is progressing in a satisfactory manner.
Each daily assessment is an opportunity to modify the monitoring regimen so as best to provide data for clinical decision making.
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Sepsis (Eg Infection Of Chest, Urinary Tract, Wound, Intravenous Cannula Site, Or Intra-abdominal Collection)
Sedative Drugs Hypoxaemia Hypercarbia Hypoglycaemia Acute Neurological Event
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Myocardial Infarction
Urinary Retention
Alcohol/Drug Withdrawal
Hepatic Encephalopathy
Biochemical Abnormality (Eg Urea, Sodium, Potassium, Calcium, Thyroid Function, Liver Function).
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Days 0-2: Mild fever (temperature <38°C) (common): Tissue damage and necrosis at the operation
site. Haematoma. Persistent fever (temperature >38°C): Atelectasis: the collapsed lung may become
secondarily infected. Specific infections related to the surgery. Blood transfusion or drug reaction.
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Days 3-5: Bronchopneumonia. Sepsis. Wound infection. Drip site infection or phlebitis. Abscess formation - eg, subphrenic or pelvic,
depending on the surgery involved. DVT.
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After 5 days: Specific complications related to surgery
eg; fistula formation.After the first week: Haemorrhage Wound infection. Distant sites of infection - eg, UTI. DVT, pulmonary embolus
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Infectious complications are the main causes of postoperative morbidity in maxillofacial surgery.
Postoperative incidence has lessened with the advent of prophylactic antibiotics but multi-resistant organisms present an increasing challenge.
Wound infection: the most common form is superficial wound infection occurring within the first week,
presenting as localised pain, redness and slight discharge usually caused by skin staphylococci.
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Cellulitis and abscesses: Most present within the first week but can be
seen as late as the third postoperative week, even after leaving hospital.
Present with pyrexia and spreading cellulitis or abscess.
Cellulitis is treated with antibiotics. Abscess requires suture removal and probing of
the wound but deeper abscess may require surgical re-exploration. The wound is left open in both cases to heal by secondary intention.
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Gas gangrene is uncommon and life-threatening.
Wound sinus is a late infectious complication from a deep chronic abscess that can occur after apparently normal healing.
It usually needs re-exploration to remove non-absorbable suture or mesh, which is often the underlying cause
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Most wounds heal without complications and healing is not impaired in the elderly unless there are specific adverse factors or complications.
Factors which may affect healing rate are: Poor blood supply. Excess suture tension. Long-term steroids. Immunosuppressive therapy. Radiotherapy. Severe rheumatoid disease. Malnutrition and vitamin deficiency.
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There are no clinical studies to indicate what is normal with respect to heart rate and blood pressure for individual patients in the postoperative period.
BRADYCARDIA A heart rate below 50 beats per minute may be normal
in a patient who is otherwise well. Correcting the slow heart rate with a vagolytic agent
(eg intravenous glycopyrronium bromide 0.2-0.4 mg or atropine sulphate 0.3- 0.6 mg) should restore the blood pressure and allow time for the cause of the low blood pressure and heart rate to be deduced.
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Heart rates over 100 beats per minute may be well tolerated by fit patients
Sustained tachycardia is particularly dangerous for patients who have documented ischaemic heart disease
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Hypotension is defined as either a systolic blood pressure of less than 100 mm Hg or as a fall of at least 25% from the patient’s normal pressure.
Hypotension is relatively common postoperatively and may be drug induced (egresidual effects
of anaesthesia, epidural or opioids) or may represent fluid deficit
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OBSERVE IF:
Awake or easily rousable Comfortable Normal preoperative BP Warm Well perfused (capillary
refill <2 seconds) Heart rate 50-100bpm Passing urine (>0.5
ml/kg/hr) No obvious bleeding
SEEK FURTHER ADVICE IF:
Drowsy or unrousable Distressed Hypertensive
preoperatively Cold Capillary refill >2 seconds Heart rate >100 or <50 bpm Oliguric (<0.5 ml/kg/hr) Signs of bleeding (drains,
wounds, haematoma)
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Hypertension is common in the postoperative period as a result of a number of factors including the stress response, pain, anxiety and failure to continue medication perioperatively.
Postoperative hypertension is associated with bleeding, cerebral events and myocardial ischaemia especially if the heart rate is also elevated.
Treatment of Hypertension Beta blockers and intravenous (IV) nitrates are
effective for the control of postoperative hypertension
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Myocardial ischaemia in the first 48 hours after an operation is the single most important predictor of serious cardiac events (including cardiac death, myocardial infarction, unstable angina, congestive heart failure and serious arrhythmias)
Several studies have demonstrated that beta blockers are effective in reducing perioperative ischaemia.
Although caution has been expressed in the general use of prophylactic beta blockade, reviews suggest that perioperative blockade reduces the incidence of both ischaemia and MI in patients undergoing high risk surgery.
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Perioperative MI (PMI) carries a high risk of both short and long term morbidity. It is usuallysilent in presentation with non-specific ECG changes
Troponin I has been shown to be a sensitive and specific method for the diagnosis of PMI,whereas Troponin T has been shown to be a marker for PMI in patients with CAD or CAD risk factors undergoing non-cardiac surgery
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Patients on warfarin sodium have increased risk of haemorrhage in the perioperative period.
Warfarin sodium should normally be discontinued preoperatively and restarted as soon as is deemed safe postoperatively
The guideline suggests that after warfarinsodium therapy is restarted following surgery it takes about three days on average for the international normalised ratio (INR) to increase above 2.0.
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Causes : Anaesthetic-impaired thermoregulation Cold operating environments Open body cavities Administration of unwarmed IV fluid. Management: Forced air warming technique (reduces
cardiac events)
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Pulmonary complications are an important and common cause of postoperative morbidity and mortality
If patients at risk can be recognised, it may be possible to modify some risk factors before elective surgery to reduce the rate of these complications
Early recognition of developing respiratory complications with appropriate interventions may improve outcome
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The generally accepted diagnostic criteria for respiratory failure, pulmonary infections, acute respiratory distress syndrome (ARDS) and acute lung injury are as follows:
Respiratory failure Type 1 PaO2 < 8kPa (60 mm Hg), PaCO2 <6.6kPa (50 mm Hg) Type 2 PaO2< 8kPa (60 mm Hg), PaCO2>6.6kPa (50 mm Hg). Atelectasis Pulmonary collapse clinically or on X-ray which may be subsegmental,
segmental, lobar or pulmonary, without evidence of respiratory infection. Respiratory infection Any two of the following on two or more days: Pyrexia >38 Positive sputum culture Positive clinical findings Abnormal chest X-ray – Atelectasis/infiltrates.
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Acute respiratory distress syndrome and acute lung injury:
Acute onset Bilateral infiltrates on chest radiography Pulmonary artery capillary wedge pressure
(PACWP) =18 mm Hg or the absence of clinical evidence of left heart failure
Acute lung injury is considered to be present if PaO2(kPa) <_ 40
ARDS is considered to be present if PaO2 (kPa) <_ 26.
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Respiratory complications occur after major surgery, particularly after general anaesthesia and can include :
Atelectasis (alveolar collapse): This is caused when airways become obstructed,
usually by bronchial secretions. Most cases are mild and may go unnoticed.
Symptoms are slow recovery from operations, poor colour, mild tachypnoea and tachycardia.
Prevention is by preoperative and postoperative physiotherapy.
In severe cases, positive pressure ventilation may be required.
Pneumonia: requires antibiotics, and physiotherapy.
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Up to 4.5% has been reported in adults; higher in children. Sterile inflammation of the lungs from inhaling gastric
contents. Presents with a history of vomiting or regurgitation with
rapid onset of breathlessness and wheezing. A non-starved patient undergoing emergency surgery is
particularly at risk. It may be of help to avoid this by crash induction
technique and use of oral antacids or metoclopramide. Mortality is nearly 50% and requires urgent treatment
with bronchial suction, positive pressure ventilation, prophylactic antibiotics and IV steroids
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Rapid, shallow breathing, severe hypoxaemiawith scattered crepitations but no cough, chest pains or haemoptysis, appearing 24-48 hours after surgery.
it occurs in many conditions where there is direct or systemic insult to the lung – eg:multipletrauma with shock.
The complication is rare and various methods have been described to predict high-risk patients.
It requires intensive care with mechanical ventilation with positive end pressure.
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Classically presents with sudden dyspnoea and cardiovascular collapse with pleuriticchest pain , pleural rub and haemoptysis.
However, smaller pulmonary emboli are more common and present with confusion, breathlessness and chest pain.
Diagnosis is by ventilation/perfusion scanning and/or pulmonary angiography or dynamic CT.
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Oxygen can be delivered by a large number of different devices.
100% oxygen can only be supplied by endotrachealintubation and positive pressure ventilation.
Oxygen should be given to patients with hypoxaemiausing a device that is best tolerated to achieve the necessary SpO2.
In normally hydrated patients humidification is unnecessary.
Failure to maintain an SpO2 >90% or PaO2>8.0 kPa is an indication to consider assisted ventilation
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BASAL REQUIREMENTS IN THE POSTOPERATIVE PATIENT
The basal requirements for young adults are approximately
30 ml/kg/day of water, 1.0-1.4 mmol/kg/day of sodium and 0.7-0.9 mmol/kg/day of potassium.
PRINCIPLES OF FLUID BALANCE As in any patient, the standard principles of fluid balance in
the postoperative patient are: to correct any pre-existing deficit
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to supply basal needs to replace unusual losses (eg from the pre-
existing surgical problem, surgical drains, pyrexia)
to use the oral route where possible; there is often an unnecessary delay in commencing oral intake after surgery
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Possible causes of volume depletion unrecognised or uncorrected preoperative
hypovolaemia (including effects of fasting) inadequate intra- or postoperative
replacement third space losses (fluid sequestration in the gut
or peritoneal cavity, oedema) drain losses fistulae
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polyuric renal failure hyperventilation pyrexia nasogastric aspirate haemorrhage inappropriate use of diuretics
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The specific consequences are: anastomotic breakdown cerebral damage renal failure multiple organ failure.
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Excessive fluid administration due to: over estimation of loss (drain or third space
losses) failure to recognise deteriorating renal function failure to recognise deteriorating cardiac
function. Volume overload can lead to pulmonary and
tissue oedema. Pulmonary oedema can be immediately life
threatening. Tissue oedema can lead to poor tissue perfusion,
failure to absorb enteral feed, and failure to eat.
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Oliguria is defined as urine volume of less than 0.5 ml/kg/hr for two consecutive hours.
Oliguria in an alert patient, is unlikely to require intervention unless it persists for four hours or more.
If oliguria is associated with fluid depletion it should be treated initially with a fluid challenge.
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In all cases of oliguria it is important to exclude obstruction of the urinary tract or urinary catheter.
Diuretics should not be used to treat oliguriaand should be reserved for fluid overload.
Dopamine should not be used to treat oliguria or to prevent renal failure
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Antidiuretic hormone (ADH) secretion is increased after surgery and if excess water is given (as 5% dextrose) then hyponatraemia may be induced.
If hyponatraemia is associated with volume depletion then there must be a degree of sodium deficiency.
The estimation of the degree of volume excess or volume depletion requires clinical assessment in addition to biochemical estimates.
Very low levels of serum sodium (110-120 mmol/L or less) can produce symptoms such as stupor, coma or fits and constitute a medical emergency
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Hypernatraemia most commonly indicates a total body deficiency of water and is an indication for prompt assessment and intervention, especially when levels exceed 155 mmol/L
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True potassium deficiency in postoperative patients may result from:
inadequate replacement renal losses endocrine abnormalities upper and lower GI losses (the actual loss of
potassium from the upper GI tract is small, butthe loss of chloride causes alkalosis which promotes the movement of potassium into cells and increases renal excretion).
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The clinical effects of hypokalaemia include skeletal muscle weakness, ileus, and cardiac arrhythmias. It can also potentiate the adverse effects of digoxin.
It is seldom necessary to replace potassium at a rate of greater than 10-20 mmol/hr.
Concentrated solutions of potassium are intensely irritant to peripheral veins and can cause tissue necrosis if they extravasate.
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Emergency treatment of hyperkalaemia: IV calcium chloride, which must be titrated
slowly, IV calcium gluconate, Nebulised beta agonists (such as salbutamol) IV 50 ml 50% dextrose with 10 units of short
acting insulin.
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Metabolic acidosis is usually due to poor tissue perfusion but can also be caused by excessive administration of saline.
A total venous bicarbonate of less than 20 mmol/L or a base deficit of greater than 4 mmol/L may indicate cause for concern, particularly if the trend is towards progressive acidosis.
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large load of acid produced endogenously as a by-product of body metabolism
acids are neutralized efficiently by several buffer systems and subsequently excreted by the lungs and kidneys
Buffers:
proteins and phosphates: primary role in maintaining intracellular pH
bicarbonate–carbonic acid system: operates principally in ECF
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buffer systems consists of a weak acid or base and the salt of that acid or base
Henderson-Hasselbalch equation, which defines the pH in terms of the ratio of the salt and acid:
pH = pK + log BHCO3 / H2CO3 = 27 mEq/L / 1.33 mEq/L = 20 / 1 = 7.4
As long as the 20:1 ratio is maintained, regardless of the absolute values, the pH will remain at 7.4
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Four types of acid-base disturbances combinations of respiratory and metabolic changes
may represent:
▪ compensation for the initial acid-base disturbance or,
▪ two or more coexisting primary disorders 10-mmHg PaCO2 change yields a 0.08 pH change
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retention of CO2 secondary to decreased alveolar ventilation
management involves prompt correction of the pulmonary defect, when feasible, and measures to ensure adequate ventilation
prevention: tracheobronchial hygiene during the postoperative , humidified air, and avoiding oversedation
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PaCO2 should not be below 30 mmHg dangers of a severe respiratory alkalosis are
those related to potassium depletion hypokalemia is related to entry of potassium ions into the
cells in exchange for hydrogen and an excessive urinary potassium loss in exchange for sodium
shift of the oxyhemoglobin dissociation curve to the left, which limits the ability of hemoglobin to unload oxygen at tissues
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Anion gap is a useful aid: normal value is 10 to 15 mEq/L unmeasured anions that account for the “gap”
are sulfate and phosphate plus lactate and other organic anions
measured ions are sodium, bicarb, and chloride
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treatment of metabolic acidosis should be directed toward correction of the underlying disorder
sodium bicarbonate is discouraged, attempt to treat underlying cause
shifts the oxyhemoglobin dissociation curve left
interference with O2 unloading at the tissue level
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common surgical patient has hypochloremic, hypokalemic metabolic alkalosis resulting from persistent vomiting or gastric suction in the patient with pyloric obstruction
unlike vomiting with an open pylorus, which involves a combined loss of gastric, pancreatic, biliary, and intestinal secretions
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majority of the 1000 to 1200g of calcium in the average-sized adult is found in the bone
Normal daily intake of calcium is 1 to 3 gm Most is excreted via the GI tract half is non-ionized and bound to proteins ionized portion is responsible for neuromuscular
stability
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signs & symptoms (serum level < 8):
numbness and tingling of the circumoral region and the tips of the fingers and toes
hyperactive tendon reflexes, positive Chvostek's sign, muscle and abdominal cramps, tetany with carpopedal spasm, convulsions (with severe deficit), and prolongation of the Q-T interval on the ECG
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causes:
▪ acute pancreatitis, massive soft-tissue infections (necrotizing fasciitis), acute and chronic renal failure, pancreatic and small-bowel fistulas, and hypoparathyroidism
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signs & symptoms:
CNS: easy fatigue, weakness, stupor, and coma
GI: anorexia, nausea, vomiting, and weight loss, thirst, polydipsia, and polyuria
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two major causes:
hyperparathyroidism and cancer
bone mets
PTH-like peptide in malignancies
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total body content of magnesium 2000 mEq about half of which is incorporated in bone distribution of Mg similar to K+, the major portion
being intracellular normal daily dietary intake of magnesium is
approximately 240 mg most is excreted in the feces and the remainder in
the urine
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causes:
starvation, malabsorption syndromes, GI losses, prolonged IV or TPN with magnesium-free solutions
signs & symptoms:
similar to those of calcium deficiency
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Symptomatic hypermagnesemia, although rare, is most commonly seen with severe renal insufficiency
signs & symptoms:
CNS: lethargy and weakness with progressive loss of DTR’s – somnolence, coma, death
CVS: increased P-R interval, widened QRS complex, and elevated T waves (resemble hyperkalemia) – cardiac arrest
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Urinary retention: this is a common immediate postoperative complication that can often be dealt with conservatively with adequate analgesia. If this fails, catheterisation may be needed, depending on
surgical factors, type of anaesthesia, co morbidities and local policies.
UTI: this is very common, especially in women, and may not present with typical symptoms. Treat with antibiotics and adequate fluid intake.
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This may be caused by antibiotics, obstructive jaundice and surgery to the aorta.
It is often due to an episode of severe or prolonged hypotension.
It presents as low urine output with adequate hydration.
Mild cases may be treated with fluid restriction until tubular function recovers. However, it is essential to differentiate it from pre-renal failure due to hypovolaemia which requires rehydration.
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In severe cases haemofiltration or dialysis may be needed while function gradually recovers over weeks or months.
One study found that factors predictive of acute kidney injury included advanced age, liver disease, high-risk surgery and peripheral vascular disease.
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Sepsis is the systemic inflammatory response to infection leading to a generalised inflammatory reaction in organs remote from the initial insult and eventually to end-organ dysfunction and/or failure
Early identification,immediate resuscitation, identifying the primary source, use of early and appropriate antibiotics and undertaking appropriate surgical drainage are the mainstays of treatment
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The response is defined by the presence of two or more of the following:
temperature >38*C or <36*C heart rate >90 beats/min respiratory rate >20 breaths/min or
PaCO2<4.3kPa white cell count >12,000 cells/mm3 , <4,000
cells/mm3, or >10% immature forms.
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Prophylactic antibiotics should be administered to appropriate groups of patients to reduce the risk of developing postoperative sepsis
Hand washing with soap and water or with alcoholic cleansing agents should be performed before and after patient contact.
Strict hand antisepsis must be achieved before the performance of invasive procedures such as surgery or the placement of intravascular catheters and indwelling urinary catheters.
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Fever/hypothermia Unexplained tachycardia Unexplained tachypnoea Signs of peripheral vasodilation Unexplained hypotension/shock Changes in mental state Leucocytosis/neutropenia Unexplained alteration in renal or liver function Thrombocytopenia/ disseminated intravascular
coagulation Metabolic acidosis
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severity of sepsis may be assessed by looking for organ dysfunction which may be reflected by altered platelet count, coagulation screen, renal function, liver function and C-reactive protein.
Urine and blood cultures should be obtained whenever there is reason to suspect systemic sepsis.
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Administration of oxygen Volume expansion using either colloid or
crystalloid. Antimicrobial therapy A course of antimicrobial treatment should
generally be limited to 5-7 days. It is important that fungi and atypical organisms
can also contribute to sepsis syndrome Surgical intervention in the form of debridement
or drainage of infected, devitalised tissue should be undertaken as soon as possible following haemodynamic stabilisation
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Malnourished patients are at increased risk of postoperative complications and mortality, yet artificial nutritional support can be associated with major complications.
Oral intake should be commenced as soon as possible after surgery
Anti-emetics should be used as required in order to promote an early return of oral intake.
All malnourished cancer patients should be considered for nutritional advice and oral supplements in the postoperative period
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For patients with ongoing postoperative complications enteral nutrition should be used whenever possible, combined with parenteral nutrition where necessary, to meet nutritional needs
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Scottish Intercollegiate Guidelines Net work 77 Postoperative management in adults
Oral and Maxillofacial Surgery: LASKIN Prevention and treatment of surgical site infection,
NICE Clinical Guideline (October 2008) Textbook of oral and maxillofacial surgery- Neelima
Malick Thompson JS, Baxter BT, Allison JG, et al ; Temporal
patterns of postoperative complications.; Arch Surg. 2003 Jun;138(6):596-602
Pile JC; Evaluating postoperative fever: a focused approach. Cleve Clin J Med. 2006 Mar;73 Suppl 1:S62-6
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Thank you....