04 Postoperative
Chest Pain
Post-operative chest pain should alert the clinician to two main diagnoses: myocardial infarction (MI) and pulmonary embolism (PE).
MI
Myocardial infarction (MI) may occur during or after the operation. The greatest risk of MI perioperatively is 48 hours after the operation. MI can be triggered by hypotension (e.g. blood loss, anesthetic vasodilation) and/or tachycardia (e.g. pain) which may result in a mismatch of myocardial oxygen supply and demand.
Diagnosis of MI during surgery is based on elevated troponin or creatinine kinase MB levels along with symptoms of ischemia or electrocardiographic (EKG) changes.
Diagnosis of MI postoperatively requires only elevated troponin or creatinine kinase MB levels without another clear etiology. Chronic elevation should be ruled out with baseline values or preoperative residual samples.
Troponin measurements are recommended in the following situations:
All patients with symptoms or EKG changes. At least two serial measurements are recommended
All patients with high cardiac risk and some with low cardiac risk (see Cardiac Risk for definition). Measurements at 6-12 hours after surgery and days 1-3 after surgery are recommended
Mortality (50%-90%) in patient with postoperative MI is much higher than MI not associated with surgery, since thrombolytics and anticoagulation are typically contraindicated in the peri-operative setting.
All patients with symptoms of ischemia or MI and all patients with high cardiac risk (see Cardiac Risk for definition) should receive 12-lead EKG.
The treatment for MI during surgery and MI postoperatively is statin and aspirin therapy.
PE
Pulmonary embolism (PE) typically occurs around post-operative day 5-7. Cancer patients and immobilized patients are at highest risk.
D-dimer is typically not useful in the post-operative period as it is very often elevated due to the surgery itself (i.e. bleeding, thrombosis, inflammatory response).
The following therapies are used to prevent atelectasis, pneumonia, and pulmonary embolism, postoperatively:
Incentive spirometry (especially in high-risk patients)
Deep breathing exercises (especially in high-risk patients)
Pain control
Physical therapy
Malignant Hyperthermia
Malignant hyperthermia is a hereditary condition induced by certain anesthetic agents characterized by massive release of intracellular calcium from the sarcoplasmic reticulum.
The inheritance of malignant hyperthermia is autosomal dominant. Malignant hyperthermia is associated with mutations in the ryanodine receptor and, less commonly, the dihydropyridine receptor.
The most common pharmacologic causes of malignant hyperthermia are:
Inhalational halogenated anesthetics (e.g. halothane)
Succinylcholine
The increased intracellular calcium within muscle cells leads to a hypermetabolic state and is a direct cause of the presenting signs and symptoms, which include:
Hyperthermia (usually very rapid, may climb 1° to 2° every 5 minutes)
Rigidity (due to sustained muscle contractions)
Tachycardia
Cyanosis
Systemic and local conditions related to unmanaged hyperthermia include:
Compartment syndrome
Myoglobinuria (due to rhabdomyolysis)
Arrhythmias (due to hyperkalemia and hypercalcemia from rhabdomyolysis)
Disseminated intravascular coagulation (DIC)
The initial step in management of malignant hyperthermia is discontinuing the offending agent. The only treatment for malignant hyperthermia is dantrolene, a muscle relaxant that disrupts excitation-contraction coupling in muscle cells. Supportive management of hyperthermia (e.g. evaporative cooling, cold inhaled O2, cold GI lavage, cool IV fluids) should be initiated as needed.
Pulmonary Aspiration
Pulmonary aspiration is the process of introducing a nonpulmonary substance to the tracheobronchial tree. Risk factors for a pulmonary aspiration include:
Altered mental status (such as sedation, neurological disorders, dementia)
Decreased gag reflex
Dysphagia
Traumatic brain injuries
Intubation and extubation
Tracheostomies
Alcoholism
Seizures
Vomiting
Esophageal problems (such as acid reflux)
Aspiration contents are usually located in characteristic locations due to the increased diameter and more vertical angle of the right bronchus compared to the left:
Upper segment of the right lower lobe (if supine)
Lower segment of the right lower lobe (if standing or sitting)
Upper segment of the right upper lobe (if patient is prone)
A pulmonary aspiration is typically diagnosed both clinically (if witnessed) and by chest x-ray.
On physical exam, patients with a pulmonary aspiration typically present with:
Wheezing
Pulse-ox desaturation
Tachypnea
Fever (classically postop day 3 pneumonia)
Dullness to percussion (if obstruction)
Crackles on auscultation
Treatment
A witnessed pulmonary aspiration may be treated by turning the patient’s head and applying suction to allow drainage of the oropharynx.
If an unwitnessed or intraoperative aspiration is suspected, supportive therapy and watchful waiting for 48 hours is useful.
Prevention of pulmonary aspiration is the best therapy:
Nil per os (NPO) preoperatively
Elevate the head of the bed
Nasogastric tube for altered mental status patients
Smoking cessation (allows for improved cilia motility)
If left untreated, a pulmonary aspiration may cause:
Chemical pneumonitis (e.g. gastric acid)
Aspiration pneumonia (e.g. oropharyngeal flora)
Lung collapse (e.g. foreign body)
Lung abscess
Pneumothorax
An intraoperative tension pneumothorax may develop in patients with weak or traumatized lungs during positive pressure ventilation (e.g. chronic tuberculosis or recent blunt trauma with broken ribs).
Classically, patients with an intraoperative tension pneumothorax become progressively harder to ventilate with deteriorating vital signs and decreased breath sounds unilaterally.
An intraoperative tension pneumothorax may be managed by needle decompression through the midclavicular second intercostal space, followed by a chest tube after stabilization.
If a tension pneumothorax develops during an abdominal surgery, needle decompression may be achieved through the diaphragm.
Fever
Causes of postoperative fever begin with malignant hyperthermia. Suspect this etiology in a patient that develops high fever (typically > 40°C (104°F)) shortly after administration of the anesthetic. IV dantrolene, 100% O2, and cooling blankets are warranted.
Bacteremia is a cause of fever within hours of the surgery. Blood cultures and empiric antibiotics are warranted.
Six “W’s” of postoperative fever:
Wonder drugs (e.g. antibiotics or heparin, most commonly)
Wonder where/why (e.g. abscess)
Wind refers to atelectasis or pneumonia and typically occurs around POD 1-2. Water refers to urinary tract infection and is commonly seen when a Foley is in place and typically occurs around POD 3-5. Walking is in reference to a deep venous thrombosis and seen around POD 4-6. Wound refers to wound infection and seen around POD 5-7. Wonder drugs refer to common medications resulting in a fever (e.g., antibiotics, chemotherapy agents, antipsychotics) seen around POD 7. Wonder why refers to a possible abscess that can be seen between POD 7-10.
Atelectasis is the most common cause of postoperative fever on days 0-1.
(Note: While the causal relationship of atelectasis and fever has been debated, the NBME still tests on this concept.)
Pneumonia is a cause of postoperative fever between days 1-3, and is typically suspected when an initial fever on postoperative day 0-1 persists for 2-3 days.
Post operative urinary tract infections typically present between postoperative days 3-5.
Thrombophlebitis may be a source of fever on postoperative days 4-6.
Postoperative wound or catheter infection usually present between postoperative days 5 to 8. The first step to treating postoperative wound infections is to remove some staples from the fluctuant wound to allow any fluid collection (e.g. pus) to drain from beneath the skin.
Drug fever should always be considered in the differential of postoperative fever, and may have a varied presentation. It can occur at any time, but classically presents on postoperative day >7.
The timing of the postoperative fever (eg, immediate, acute, subacute, delayed) also suggests the likely diagnosis. Fever occurring immediately (within a few hours) in the operative or postoperative period is typically due to prior infection or trauma, inflammation due to surgery, malignant hyperthermia, or medications (eg, anesthetics) or blood products given during or prior to surgery. Acute fever (within the first week after surgery) is most often caused by nosocomial infections (eg, pneumonia, urinary tract infection) or other noninfectious causes such as pulmonary embolus (PE). Subacute fever (>1 week after surgery) is usually due to drug fever, surgical site infection, or PE. Delayed postoperative fever is typically caused by an infection (eg, viral infections from blood products, infective endocarditis).
Drug fever is typically a diagnosis of exclusion. It is often associated with use of anticonvulsants, antibiotics (beta-lactams, sulfonamides), or allopurinol.
Atelectasis
Atelectasis is lobar or segmental collapse of the lung that causes decreased lung volume. It is classified by pathophysiology (obstructive or nonobstructive), location, and amount of involved lung.
Postoperative atelectasis is usually due to accumulation of pharyngeal secretions, the tongue prolapsing posteriorly into the pharynx, airway tissue edema, or residual anesthetic effects. Postoperative pain can also interfere with spontaneous deep breathing and coughing, which decreases the functional residual capacity and worsens the atelectasis. Atelectasis is more common following abdominal and thoracoabdominal procedures. Large areas of atelectasis may cause significant ventilation-perfusion mismatch, leading to hypoxemia and increased work of breathing (eg, dyspnea, tachypnea). These manifestations typically start after the patient has left the post-anesthesia care unit, become most severe during the second postoperative night, and can last up to 5 days.
As compensation for the hypoxemia, patients usually hyperventilate and develop respiratory alkalosis and decreased arterial partial pressure of carbon dioxide (PaCO2). Acute pulmonary embolism can occur postoperatively and present with similar arterial blood gas (ABG) levels.
Pulmonary
abx not useful to prevent pneumonia. Only use abx if obvious infections or emergency surgery
COPD/asthma patients: controll with glucocorticoids/beta agonists. Delay elective surgery. Use preoperative glucocorticoids if uncontrolled and emergent surgery
Ileus
A postoperative paralytic ileus refers to the severe constipation and overall intestinal atony following an abdominal or non-abdominal surgery.
Postoperative paralytic ileuses are typically benign, occurring anywhere from the stomach through the large intestines as a result of:
Inflammatory responses to mechanical movement or trauma
Inhibitory neural reflexes within the sympathetic ganglia
Nitric oxide and VIP inhibitory peptide release
Opioid medications
Hypokalemia, hypomagnesemia
Acute colonic pseudo-obstruction (aka Ogilvie's syndrome) should be suspected in severely ill patients with a dilated cecum and right hemicolon and is typically managed through supportive therapy and neostigmine.
Risk factors for a postoperative paralytic ileus include:
Abdominal or pelvic surgery
Prolonged surgical time
Open surgery (versus laparoscopic)
Obesity
Transfusions
Perioperative intestinal inflammation
Contributors to PPI include increased splanchnic nerve sympathetic tone following peritoneal instrumentation, local release of inflammatory mediators, and postoperative opiate analgesic use (which causes decreased gastrointestinal motility and disordered peristalsis). Techniques to prevent PPI include epidural anesthesia, minimally invasive surgery, and judicious perioperative use of intravenous fluids (to minimize gastrointestinal edema). Diagnosis is clinical, although abdominal x-rays revealing dilated loops of bowel with no transition point support the diagnosis.
Symptoms
Patients with a postoperative paralytic ileus symptomatically present with:
Abdominal distention
Nausea
Vomiting
Intolerance to oral foods/drinks
Delayed flatulence or stool passage
Pain
Patients with a postoperative paralytic ileus typically present with the following physical exam findings:
Abdominal distention
Tympanic on percussion
Diffuse tenderness
Decreased bowel sounds (vs. small bowel obstruction which has increased bowel sounds)
Diagnosis
The diagnosis of a postoperative paralytic ileus is typically a diagnosis of exclusion, however an abdominal x-ray may be used to rule out obstruction.
Classically on abdominal imaging, patients with a postoperative paralytic ileus demonstrate:
Dilated bowel loops (x-ray)
Free air in the colon (x-ray)
No transition zone (CT)
Notably, a mechanical small bowel obstruction will have an identifiable transition zone on abdominal CT, in contrast to ileus.
Management
The management of a postoperative paralytic ileus is typically supportive therapy including:
Correcting electrolyte abnormalities
Weaning off pain medications
Bowel rest
Laxatives such as docusate (Colace, Dulcolax)
Acute colonic pseudo-obstruction (aka Ogilvie's syndrome) should be suspected in severely ill patients with a dilated cecum and right hemicolon and is typically managed through supportive therapy and neostigmine.
Urinary Retention
Urinary retention is common problem postoperatively. Risk factors for postoperative urinary retention include:**
Pain medications (e.g. opioids)
Anticholinergic medications
Spinal anesthesia
Long duration of anesthesia
Pelvic surgeries/manipulation (e.g. rectal stimulation can reflexively inhibit bladder contraction)
Postoperative day 1 - 3
Postoperative urinary retention is common after surgery in the abdomen, pelvis, rectum, or groin. Patients will present with:
Urgency
Discomfort
Fullness on palpation of bladder
Inability to void
The first step in managing a postoperative patient with bladder distention and urinary retention is “in and out” catheterization (straight catheterization).
Patients with low urinary output, less than 0.5mL/kg/hour, who have had urinary retention ruled out via straight or current indwelling catheterization in the presence of normal perfusing blood pressure should be worked up to rule out dehydration or acute renal failure.
Fluid challenge (bolus of 1 liter of normal saline) is an appropriate first step in the evaluation of a postoperative patient with oliguria without urinary retention. Urine output will increase in a dehydrated patient with prerenal azotemia and will remain the same in patients with renal failure.
Urinary sodium less than 20 mEq/L is suggestive of dehydration while more than 40 mEq/L is suggestive of acute renal failure.
Wounds
The four types of wounds include:
Clean
Clean-contaminated
Contaminated
Dirty
A clean wound is defined as atraumatic and having no gastrointestinal (GI), genitourinary (GU), or respiratory tract involvement. An example is surgical incision.
A clean-contaminated wound is similar to a clean wound, but with GI, GU, or respiratory tract involvement. An example is a minor sterile break into the GI, GU, or respiratory tracts.
A contaminated wound is direct contact of GI, GU, or respiratory contents with wound. An example is traumatic wound with GI, GU, or respiratory matter.
A dirty wound is active infection within wound. An example is infected surgical wound with abscess.
The four types of wound healing include:
Primary intention
Secondary intention
Delayed primary closure
Skin grafts
Wound healing by primary intention refers to any technique where the epidermal edges of the wound are approximated. Examples include the surgical incisions or lacerations closed with staples, sutures, or adhesive.
Wound healing by secondary intention leaves the wound open. These wounds are treated with "wet-to-dry" dressings. Examples include subcutaneous abscess after incision and drainage and open appendectomy for perforated appendicitis.
Delayed wound closure (or wound healing by tertiary intention) is left to heal by secondary intention for up to 5 days then the wound edges are approximated and closed as in wound healing by primary intention. This type of wound healing is possible due to the highly vascular granulation tissue of secondary intention wound healing making it more resistant to infection.
Wound healing with skin grafts refers to the use of split-thickness skin grafts consisting of epidermis and a portion of dermis.
Dressings are required for open wounds for the first 48 hours after closure.
Delayed Healing
Systemic factors that may inhibit and/or delay wound healing are:
Malnutrition
Corticosteroids
Smoking
Hepatic and/or renal failure
Diabetes mellitus
Local factors that may inhibit and/or delay wound healing are:
Radiation
Infection
Bleeding/hematoma (can lead to infection)
Improper wound management (e.g. not keeping the wound clean, debrided, dry, closed)
Wound Dehiscence
Wound dehiscence is when a wound breaks open along surgical suture, typically occurs around post-operative day 5.
Wound dehiscence can appear to be intact, but large amount of “salmon-colored” (peritoneal) fluid soaks the dressing.
The most common cause of wound dehiscence is wound infection.
Wound dehiscence requires re-operation to prevent evisceration.
Surgery may not be necessary in cases where only part of the incision has opened and where the fascia remains intact. To assess whether the patient needs surgery, sutures or staples must be removed from the affected portion of the incision and the wound must be probed with cotton-tipped applicators.
Fistula
A gastrointestinal fistula usually occurs as a complication of abdominal surgery and is often recognized when bowel contents leak through a surgical wound or drain site.
Most will heal in several weeks; however, when fistulas fail to heal use the FRIEND mnemonic to remember possible explanations:
Foreign body in the wound
Radiation damage
Infection or Inflammatory bowel disease
Epithelialization of the fistulous tract
Neoplasm
Distal bowel obstruction
General management of a freely draining fistula centers on ordering NPO status, fluid and electrolyte replacement, and intensive protection of the abdominal wall to prevent erosion.
Transfusion reactions
Bacterial Parotitis
This patient's fever, leukocytosis, and parotid inflammation suggest acute bacterial parotitis. Dehydrated post-operative patients and the elderly are most prone to develop this infection. Acute bacterial parotitis presents with painful swelling of the involved parotid gland that is aggravated by chewing. Prominent physical exam findings are a tender, swollen and erythematous gland; with purulent saliva expressed from the parotid duct. The most common infectious agent is Staphylococcus aureus. Adequate fluid hydration and oral hygiene, both pre- and post-operatively, can prevent this complication.
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