3. Introduction
ď§ Surgical complications constitute a frustrating and difficult aspect of
the operative treatment of patients
ď§ Regardless of how technically gifted and capable of surgeons are, all
will have to deal with complications.
ď§ Complications can occur for various reasons
oSurgeon related factors
oPatient related factors
o nature of disease
oProphylactive antibiotics
4. Surgical wound complication
a) seroma
⢠Collection of liquefied fat, serum and lymphatic fluid under the incision.
⢠Occur In large skin flaps( mastectomy, axillary dissection, groin dissection
and large ventral hernia or
⢠when a prosthetic mesh (polytetrafluoroethylene) is used in the repair of a
ventral hernia.
⢠Most benign complication
⢠Presentation
⢠Localized swelling
⢠Pressure or discomfort
5. ⢠Treatment
- sterile aspiration & pressure dressings
- open drainage
-failure of aspiration 2x
-infected seroma
-mesh+seroma
-infected mesh+seroma âremove mesh
⢠Prevention
-place drain under skin
-avoid premature removal of drain
-pressure dressings
6. b)Hematoma
⢠An abnormal collection of blood usually in a subcutaneous layer of incision or in potential
space in the abdominal cavity
⢠Has a potential for super infection
⢠Results due to inadequate hemostasis, depletion of clotting factors and presence of
coagulopathy .
⢠C/f may vary with its size, location, and presence of infection.
⢠In the neck, a large hematoma may cause compromise of the airway;
⢠In the retroperitoneum, it causes paralytic ileus, anemia, and
ongoing bleeding caused by local consumptive coagulopathy; and
⢠in the extremity and abdominal cavity, it may result in compartment syndrome.
⢠P/E localized soft swelling with purplish blue discoloration of the overlying skin/
drainage of dark red fluid from the fresh wound.
7. o Prevention
ď§ Discontinuing medications that alter coagulation
-Warfarin must be discontinued 4 to 5 days before surgery resumed 12 to 24 hrs after surgery
-IV UFH can be discontinued 4 hrs before surgery
ď§ correcting coagulation abnormality
-LMWH discontinued 16 to 24 hrs before surgery resumed 48 to 72 hrs post operatively
-ASA and clopidogrol must be withhold 6 to 7 days before and resumed after 24hrs of surgery
o Treatment
ď§ Small hematomas - eventually resorb
ď§ Most retroperitoneal hematoma - expectant management
ď§ Large expanding neck hematoma - evacuated at OR after securing the air way
8. c) Acute wound failure(dehiscence)
⢠postoperative separation of the abdominal musculoaponeurotic layers.
⢠Wound dehiscence is among the most dreaded complications faced by
surgeons and is of great concern because of the risk of evisceration; the
need for some form of intervention; and the possibility of repeat
dehiscence, surgical wound infection, and incisional hernia formation.
⢠Acute wound failure occurs in approximately 1% to 3% of patients who
undergo an abdominal operation.
⢠Dehiscence most often develops 7 to 10 days postoperatively but may
occur anytime after surgery (range, 1 to >20 days).
9.
10. ⢠Presentation
⢠Evisceration
⢠25% salmon colored fluid
⢠Prevention
⢠Proper spacing of suture
⢠Adequate depth of bite of the fascia
⢠Relaxation during closure
⢠Tension free closure
11. ďąTreatment
ď§ Small dehiscence - can be treated by conservatively with saline
moistened gauze packing of the wound & use of abdominal binder.
ď§ If evisceration-explore abdominal cavity for septic focus &leakage
ď§ If fascia is strong and intact - primary closure
⢠If necrotic or infected- debridement &incision closed by retension suture
⢠for high risk patient interrupted suture is wisest
⢠Skin graft
12. d) Surgical site infection(wound infection)
ď§ Surgical site infections (SSIS) are infections of the tissues, organs, or spaces exposed by surgeons
during performance of an invasive procedure.
SSIS are classified into
1) incisional SSI- a) superficial SSI - skin and subcutaneous tissue
b) deep incisional SSI-muscle and fascia
2) organ/space infections - the internal organs of the body if the operation includes that area.
The development of SSI is related to three factors:
(A) the degree of microbial contamination of the wound during surgery;
(B) the duration of the procedure; and
(C) host factors such as diabetes, malnutrition obesity, immune suppression;
13.
14. SSIs most commonly occur 5 to 6 days postoperatively but may
develop sooner or later than that.
Approximately 80% to 90% of all postoperative infections occur within
30 days after the operative procedure
C/f erythema, tenderness, edema, and occasionally drainage.
The wound is often soft or fluctuant at the site of infection,
Ix -leukocytosis and a low-grade fever
15. ⢠According to The Joint Commission, a surgical wound is considered
infected if
⢠(1) grossly purulent material drains from the wound,
⢠(2) the wound spontaneously opens and drains purulent fluid,
⢠(3) the wound drains fluid that is culture-positive or Gram stainâ
positive for bacteria, and
⢠(4) the surgeon notes erythema or drainage and opens the wound
after determining it to be infected.
16.
17.
18. Prevention
⢠Prevention - relies on changing or dealing with modifiable risk factors for
SSI
-Stop smoking 30 days prior to surgery
-Control of blood glucose in diabetics
-Malnourished pts nutritional supplements 7 to 14 days prior to surgery
-Obese patients encouraged to weight loss prior to surgery
- Corticosteroid wined of or decrease the dose,
-bowel preparation, prophylactic Abcs,
-Intraoperative steps are important
19. Treatment
Treatment depends on the depth of infection
⢠If fascia is intact debridement and irrigation, pack to its base with saline-moistened gauze
⢠if wide spread cellulitis with significant signs of infection, IV abcs
⢠If dehiscence or intra abdominal abscess ,drainage and reoperation
⢠A deep SSI associated with grayish, dishwater-colored fluid and frank necrosis of the
fascial layer raise suspicion for the presence of a necrotizing type of infection.
⢠The presence of crepitus in any surgical wound or gram-positive rods (or both) suggests
the possibility of infection with C. perfringens.
-Rapid and expeditious surgical dĂŠbridement is indicated in these
settings.
20. COMPLICATIONS OF THERMAL REGULATION
A)hypothermia
⢠More than 80% of elective operative procedures are associated with a
decrease in body temperature, and
⢠50% of trauma patients are hypothermic on arrival in the operating suite.
⢠Causes,
ď§ Rapid resuscitation with cool iv fluids,
ď§ Transfusions,
ď§ Intracavitary irrigation with cold irritant,
ď§ Prolonged surgical procedure,
ď§ Anesthesia
ď§ Opioid analgesics
ď§ Paralysis
21. ⢠PRESENTATION
o increased early postoperative ischemia
oincrease in ventricular tachyarrhythmia.
opoor wound healing and infection.
o relative diuresis, compromised hepatic function, and some
neurologic manifestation
oIn severe cases, the patient can have significant cardiac slowing and
may be comatose, with low blood pressure, bradycardia, and a very
low respiratory rate
22. TREATMENT
1) Infusion of iv fluids and blood through a warm device
2) Heating and humidification of inhalational gases
3) Immediate placement of warm blankets
4) Peritoneal lavage with warmed fluids
5) Rewarming infusion devices with arteriovenous system
6) Rare case cardiopulmonary bypass
23. b) Malignant Hyperthermia
⢠Is a life threatening hyper metabolic crisis manifested during or after
exposure to a triggering general anesthetic in susceptible individuals
⢠An autosomal dominant disease
⢠Mutation result in altered calcium regulation in skeletal muscles resulting
in efflux of ca2+ from sarcoplasmic reticulum to myoplasm
⢠which leads to prolonged activation of muscle filaments, culminating in
rigidity and hyper metabolism
⢠Un controlled glycolysis & aerobic metabolism give rise to cellular hypoxia,
lactic acidosis,& hypercapnia results in excessive generation of heat.
25. ⢠Treatment
ďźDiscontinue triggering anesthetic
ďźHyper ventilation with 100% oxygen
ďźAdminister alternative anesthesia
ďźTerminate surgery
ďźGive dantroline antidote
ďźsurface cooling
ďźBicarbonate for acidosis
ďźB âblockers, lidocaine, diuretics,
ďźManagement of electrolyte abnormalities
26. Management of Malignant Hyperthermia
⢠Discontinue the triggering anesthetic.
⢠Hyperventilate the patient with 100% oxygen.
⢠Administer alternative anesthesia.
⢠Terminate surgery.
⢠Give dantrolene, 2.5 mg/kg, as a bolus and repeat every 5 minutes, then 1 to2 mg/kg/hr until normalization or
disappearance of symptoms.
⢠Check and monitor arterial blood gas and creatine kinase, electrolyte, lactate,and myoglobin levels.
⢠Monitor the ECG, vital signs, and urine output.
⢠Adjunctive and supportive measures are carried out:
⢠Volatile vaporizers are removed from the anesthesia machine.
⢠Carbon dioxide canisters, bellows, and gas hoses are changed.
27. ⢠Surface cooling is achieved with ice packs and core cooling with cool
Parenteral fluids.
⢠Acidosis is monitored and treated with sodium bicarbonate.
⢠Arrhythmias are controlled with beta blockers or lidocaine.
⢠Urine output more than 2 ml/kg/hr is promoted; furosemide (lasix) or
Mannitol and an infusion of insulin and glucose (0.2 U/kg in a 50%
Glucose solution) are given for hyperkalemia, hypercalcemia, and
Myoglobulinuria.
⢠The patient is transferred to the icu to monitor for recurrence.
28. c)POSTOPERATIVE FEVER
- Fever after surgery is reported to occur in up to two thirds of patients,
and
⢠Infection is the cause of fever in about a third of cases.
⢠The most common infections
- Surgical site infection
- Urinary tract infection
- Pneumonia
- Intravascular catheterârelated infection
29.
30. ⢠High fever that fluctuates or is sustained and that occurs 5 to 8 days
after surgery is more worrisome than fever that occurs early
postoperatively.
⢠In the first 48 to 72 hours after abdominal surgery, atelectasis is often
believed to be the cause of the fever.
⢠Occasionally, clostridial or streptococcal surgical site infections can be
manifested as fever within the first 72 hours of surgery
31. - Evaluation involves studying the six W's:
- Wind (lungs)
- water (urinary tract)
- Walk (e.g., thrombosis)
- Wound (ssi
- Waste (lower GI tract)
- Wonder drug (e.g., antibiotics)
- Clinical assessment â HX and PE
32. âWindâ âWaterâ âWalkâ âWoundâ
Atelec
tasis
Day
1
Pneu
monia
Day 3
UTI
Day 3
DVT
Day 5
Wound
Infecti
on
Day 7
Deep
Abscess
Day 10
POSTOPERATIVE DAY
POSTOPERATIVE FEVER BY PO DAY
33. ďą investigation
⢠Blood culture
⢠CBC
⢠Urinalysis and culture
⢠CXR
⢠Echocardiography
⢠abdominal u/s, and CT scan
ďąTreatment
⢠antipyretics are recommended
⢠Antibiotics if infection presents
34. RESPIRATORY COMPLICATIONS
⢠Loss of functional residual capacity is present in almost all patients
⢠This loss may be the result of abdominal distention, painful upper abdominal
incision, obesity, strong smoking history with associated chronic obstructive
pulmonary disease, prolonged supine positioning, fluid overload ,anesthesia and
narcotics
⢠Vital capacity may be reduced 50% of normal for the first 2 days after surgery for
reasons that are unclear
⢠The overall incidence of pulmonary complications exceeds 25% in surgical
patients.
⢠Of all postoperative deaths, 25% are caused by pulmonary complications, and
pulmonary complications are associated with 25% of the other lethal
complications.
35. a) Atelectasis
⢠Is the most common post operative respiratory complication ,results
in a loss of (FRC) of the lung
⢠Predispose to pneumonia
⢠Most common Cause of post operative fever in the first 48 hrs
⢠As a result of the anesthetic, abdominal incision, and postoperative
narcotics, heavy smokers, obese, and have copious pulmonary
secretionss.
⢠Patients present with a low-grade fever, malaise, and diminished
breath sounds in the lower lung fields.
36. 1. Preop prophylaxis:
a. No smoking (2 wks)
b. Treatment of pulmonary problem
2. Postop prophylaxis:
â Minimal use of depressant drugs
â Prevent pain
â Early ambulation
â Changes body position
â Deep breathing and coughing exercises
3. Drugs:
a. Expectorants
b. Mucolytic
c. Bronchodilators
37. b)Aspiration pneumonia/pneumonitis
⢠Aspiration pneumonitis - is acute lung injury that results from the
inhalation of regurgitated gastric contents
⢠Aspiration pneumonia - inhalation of oropharyngeal secretions that
are colonized by pathogenic bacteria
⢠Risk factors- impairment of the esophageal sphincter and laryngeal
reflexes, altered GI motility, absence of preop fasting, emergency
surgery, altered consciousness, trauma patients, DM patients etc
38. ďAspiration Pneumonitis patients:
ď§ have associated vomiting
ď§ are obtunded or have altered consciousness
ď§ have initially wheezing and labored respiration then cough
Others have cough, shortness of breath, and wheezing that
progressively progress to pulmonary edema and ARDS
ďAspiration pneumonia
CXR - Infiltrates in posterior segment of the upper lobes and the apical
segments of the lower lobes.
39. Management
⢠Postoperatively, it is important to avoid the overuse of narcotics, encourage the patient
to ambulate, and cautiously feed a patient who is obtunded, elderly, or debilitated.
⢠A patient who sustains aspiration of gastric contents needs to be immediately placed on
oxygen and have a chest radiograph to confirm the clinical suspicions
⢠Close surveillance of the patient is absolutely essential
⢠If the patient is maintaining oxygen saturation via facemask without an excessively high
work of breathing, intubation may not be required
⢠After intubation for suspected aspiration, suctioning of the bronchopulmonary tree will
confirm the diagnosis and remove any particulate matter
⢠Administration of empirical antibiotics is also indicated in a patient with aspiration
pneumonitis that does not resolve or improve within 48 hours of aspiration
40. c)Pulmonary edema, ALI and ARDS
⢠Pulmonary edema
⢠Accumulation of fluid in the alveoli
⢠Usually due to increased vascular hydrostatic pressure associated with CHF & acute
myocardial infarction (MI)
⢠It is also commonly associated with fluid overload as a result of overly aggressive
resuscitation
⢠increased pulmonary capillary wedge pressure (PCWP) and right-sided heart
pressure
⢠ALI and ARDS -associated with hypo-oxygenation b/s of a pathophysiologic
inflammatory response that leads to the accumulation of fluid in the alveoli &
thickening in the space between the capillaries and the alveoli.
41. ⢠Acute lung injury â a pao2/ FIO2 ratio of less than 300,
-Bilateral infiltrates on chest radiograph, and
-PCWP less than 18 mm hg.
- It tends to be shorter in duration and
Not as severe.
⢠ARDS is associated with - pao2/fio2 ratio of less than 200 and
-has bilateral infiltrates and
- PCWP less than 18 mm hg
42. Clinical Presentation
⢠Patients with pulmonary edema often have a corresponding cardiac
history or a recent history of massive fluid administration.
⢠Patients with acute lung injury and ARDS generally have tachypnea,
dyspnea, and increased work of breathing, as manifested by exaggerated
use of the muscles of breathing.
⢠Cyanosis is associated with advanced hypoxia and is an emergency.
⢠Auscultation of the lung fields reveals crackles and
⢠Arterial blood gas analysis will reveal the presence of a low Pao2 and a
high Paco2.
43. Management
⢠Patients with pulmonary edema are managed by fluid restriction and
aggressive diuresis.
⢠Administration of oxygen via facemask in mild cases and intubation in
more severe cases is also clinically indicated.
⢠In most cases, the pulmonary edema resolves quickly after diuresis
and fluid restriction.
⢠In patients with impending respiratory failure, including tachypnea,
dyspnea, and air hunger, management of acute lung injury and ARDS
is initiated by immediate intubation plus careful administration of
fluids.
44. d)Venous Thromboembolism
⢠Venous thromboembolism is caused by a perturbation of the
homeostatic coagulation system induced by intimal injury, stasis of
blood flow, and a hypercoagulable state.
⢠The majority of pulmonary emboli originate from an existing dvt in
the legs, and
⢠Iliofemoral venous system is the site from which most clinically
significant pulmonary emboli arise.
⢠PE develops in about 50% of patients with proximal dvt.
45. More than 50 % are silent DVT manifesting as PTE
⢠Most symptoms and signs associated with symptomatic PE are
nonspecific.
⢠Pleuritic chest pain, cough, hemoptysis, Sudden dyspnea
⢠Tachypnea, tachycardia, leg swelling
46. Diagnosis
⢠CXR
⢠D-dimer
⢠Echocardiography
⢠Pulmonary angiography is the gold standard
⢠Echocardiography
⢠ECG
⢠Venous Ultrasound of the leg
⢠Helical CT
47. ďąTreatment
⢠Non pharmacologic :
⢠elastic stockings,
⢠intermitent pneumatic compression devices,
⢠venous foot pumps,
⢠inferior venacava filter
⢠Oxygen administration
⢠In massive PE resuscitation, enhance coronary blood flow, decrease RV ischemia
⢠Anticoagulant heparin
⢠80 IU/kg bolus
⢠Followed by 18 IU/kg/ hr continuous infusion
⢠Overlapped with warfarin
2-5 mg q day
⢠Thrombolytic / embolectomy
48. Cardiac complications
A) HYPERTENSION
Perioperative hypertension (or hypotension) occurs in 25% of patients
undergoing surgery.
The risk of hypertension is related to the type of surgery performed
and the presence of perioperative hypertension.
Cardiovascular, thoracic, and intra abdominal procedures are most
commonly associated with hypertensive events.
49. Causes
⢠Pain,
⢠Hypothermia,
⢠Hypoxia,
⢠Fluid overload,
⢠Discontinuation of chronic anti hypertensive medications,
⢠Intra abdominal bleeding,
⢠Head trauma,
⢠Pheochromocytoma
ďąTreatment
⢠adequate analgesia,
⢠antihypertensive medications,
⢠avoid fluid overload, hypoxia, hypothermia
50. b) Myocardial ischemia and infarction
⢠Post-operative myocardial complications result in at least 10% of all post-
operative deaths.
⢠Patients at risk for an acute cardiac event in the post-operative period are the
elderly, those with peripheral artery disease, and patients undergoing vascular,
thoracic, major orthopedic, and upper abdominal procedures.
⢠The risk for myocardial ischemia and MI is greatest in the first 48 hours after
surgery, and it may be difficult to make the diagnosis.
⢠The classic manifestation, chest pain radiating into the jaw and left arm region, is
often not present.
⢠Patients may have shortness of breath, an increased heart rate, hypotension, or
respiratory failure
51. Treatment
⢠Prevention is the most important part of the management
⢠Preoperative cardiac risk assessment includes adequate history taking,
physical examination, and basic diagnostic tests
⢠Patients identified as being at high risk for myocardial events in the
perioperative period are managed with
⢠β-blockers
⢠Careful monitoring intra-operatively
⢠Maintenance of perioperative normothermia and vital signs
⢠Continued pharmacologic management postoperatively, including the
administration of adequate pain medication
⢠An ECG is obtained before, immediately and 2 days after surgery
52. c)Cardiac arrhythmias
⢠Common in the postoperative period and are more likely to occur in
patients with structural heart disease.
⢠Cardiac arrhythmias are classified into tachyarrhythmia,
bradyarrhythmia, and heart block.
⢠Sinus tachycardia and atrial flutter/fibrillation are the most common
types of tachyarrhythmias
⢠Sinus tachycardia is caused by pain, fever, hypovolemia, anemia, anxiety, and less
commonly, heart failure, MI, thyrotoxicosis, and pheochromocytoma.
⢠Atrial flutter/fibrillation occurs commonly in patients with electrolyte imbalance,
a history of atrial fibrillation, and chronic obstructive lung disease.
53. Presentation and Treatment
⢠Most arrhythmias are transient and benign and are not associated with
symptoms or physiologic changes.
⢠Symptoms associated with arrhythmias include palpitations, chest pain,
shortness of breath, dizziness, loss of consciousness, cardiac ischemia, and
hypotension.
⢠Tachyarrhythmia: β-blockers or alternatives (digoxin, calcium channel
blockers,amiodarone,lidocaine,procaine amide)
⢠Bradyarrythmia,
⢠If sustained atropine,or b-adrenergic agonist
⢠Heart block,
⢠Insertion of permanent pacemaker, anticoagulant
54. d)Heart failure
⢠Risk factors are
⢠MI ,
⢠volume overload,
⢠hypertension,
⢠sepsis,
⢠occult valvuar disease,
⢠PE,
⢠decompression of pre existing heart failure
⢠Higher during the first 24 to 48 hrs of surgery
⢠Treatment âoptimizing preload, afterload and myocardial contractility
55. GASTROINTESTINAL COMPLICATIONS
A) early postoperative bowel obstruction
⢠Denotes obstruction occurring within 30 days after surgery.
⢠Can be a) functional ( Ileus), caused by inhibition of propulsive bowel activity, or
⢠B) mechanical as a result of a barrier
⢠Primary or postoperative ileus - occurs immediately after surgery in the absence of
precipitating factors and resolves within 2 to 4 days
- affects the stomach and colon primarily
⢠secondary(adynamic or paralytic )ileus- occurs as a result of a precipitating
factor and is associated with a delay in return of bowel function
- the stomach, small bowel, and colon are affected.
56. Causes of Intestinal Paralytic Ileus
⢠Intra-abdominal infection (peritonitis or abscess)
⢠Retroperitoneal hemorrhage and inflammation
⢠Electrolyte abnormalities
⢠Lengthy surgical procedure and prolonged exposure of abdominal
contents
⢠Medications (e.G., Narcotics, psychotropic agents)
⢠Pneumonia
⢠Inflamed viscera
⢠Pancreatitis
57. ⢠Mechanical bowel obstruction - luminal, mural, or extraintestinal barrier.
⢠can be1) partial-anterograde contraction-defecation
2) high grade(total) âretrograde contraction-vomiting
or
1) proximal part of the small bowel (high obstruction) or
2)distal part of the small bowel (low obstruction),
or
1) closed-loop or
2) open-ended obstruction
58. ⢠clinical manifestations varies with the
-cause,
-degree, and
-level of obstruction.
⢠Patients with high mechanical small bowel obstruction
- vomit early in the course and usually have no or minimal distention.
- vomitus is generally bilious.
⢠Patients with distal obstruction vomit later in the course and have
⢠more pronounced abdominal distention.
⢠vomitus may initially be bilious and then becomes more feculent
60. Paralytic ileus Mechanical obstruction
Diffuse discomfort Sharp, colicky pain
Distended quite abdomen with few bowel sounds high pitched ,tickling sounds
Diffusely dilated bowel through out intestinal tract. Air-
fluid levels may be present, and the amount of dilated
bowel varies greatly
Small bowel dilation with air fluid levels &
thickened valvulae conniventes in the bowel proximal
to the point of obstruction and
air in the colon and rectum little or no gas in the bowel distal to the obstruction.
Differentiation between adynamic ileus and mechanical obstruction is
imperative because the treatment is completely different
62. ⢠Emergency relaparotomy - closed-loop, high-grade, or complicated
small bowel obstruction, intussusception, or peritonitis.
⢠Adynamic ileus -resolving the precipitating factors and expectantly
waiting for resolution, with surgery not usually being required.
⢠Partial mechanical small bowel obstruction -initially managed
expectantly and for a longer period, 7 to 14 days, if the patient is stable
and clinical and radiologic improvement continues.
⢠During this time nutritional support is initiated and surgical intervention is
performed if there are signs of deterioration or no improvement
63. b)Acute Abdominal compartment syndrome
⢠ACS comprises increasing organ dysfunction or failure as a result of
IAH.
⢠IAH is present when there is consistent increased IAP greater than 12
mm Hg
⢠ACS develops when IAP is 20 mm Hg or greater, with or without
abdominal perfusion pressure less than 50 mm Hg ;
⢠it is associated with failure of one or more organ systems that was not
present previously
⢠Primary ACS develops as a result of pathologic IAH caused by intra-
abdominal pathology-
64. causes
ďą Multiple trauma, especially after damage control surgery,
ďą Ileus caused by -bowel edema and contamination,
- continued bleeding, coagulopathy,
--packing used to control bleeding,
-Capillary leak, and massive fluid resuscitation and transfusion.
ďą Closure of a noncompliant abdominal wall under tension
ďą in nontrauma patients
⢠Ascites,
⢠Retroperitoneal hemorrhage,
⢠Pancreatitis, or pneumoperitoneum
⢠reduction of chronic hernias that have lost their domain,
⢠Repair of ruptured abdominal aortic aneurysm,
⢠Complex abdominal procedures, and
⢠Liver transplantation.
65. secondary ACS
ď§ develops in the absence of intra-abdominal primary pathology, injury,
or intervention.
ď§ is in part iatrogenic and
ď§ commonly encountered in patients with
o shock requiring aggressive fluid resuscitation with crystalloids,
othermally injured and shock trauma victims,
ocritically ill hypothermic and septic patients, and
opatients who have sustained cardiac arrest.
66. Presentation
⢠Patients with ACS have difficulty breathing or are difficult to ventilate and
exhibit increasing PAP, decreased volumes, hypoxia, worsening
hypercapnia, and deteriorating compliance.
⢠Co is reduced, despite apparent high filling pressures, and vasopressor
therapy is required.
⢠Abdomen becomes distended and tense, and
⢠Neurologic deterioration may occur.
⢠Central venous pressure, pcwp, and pap become elevated, and
⢠acidosis develops.
⢠Anuria, exacerbation of pulmonary failure, cardiac decompensation, and
death ultimately occur.
67. ⢠Use of the urinary bladder catheter has been the gold standard and is
the indirect method used to measure IAP.
⢠Once measured, the pressure is graded:
GI (IAP <10-15 CMH2O)
GII(IAP<16-25CmH20)
GIII(IAP<26-35CmH20)
GIV(IAP>36 CmH20)
68. ⢠Conservative fluid resuscitation;
⢠administration of analgesia, sedatives, and
⢠pharmacologic paralysis;
⢠patient positioning;
⢠drainage of intra-abdominal fluid;
⢠escharotomy;
⢠renal placement therapy; and diuretics are measures that may
prevent progression to ACS
69. Indication for decompression
⢠grade III IAH with tense abdomen and signs of extreme ventilatory
dysfunction and oliguria .
⢠grade IV IAH, with signs of ventilator and renal failure,
⢠In patients with severe head injury and IAP greater than 20 mm Hg,
even without overt ACS, or intractable intracranial hypertension
without obvious head injury
70. c)Postoperative Gastrointestinal Bleeding
⢠Postoperative GI bleeding is one of the most worrisome complications
encountered by general surgeons
ďą Causes
⢠peptic ulcer disease,
⢠Stress erosion,ulceration
⢠Mallory-weiss tear,
⢠Gastric varices;
⢠Arteriovenous malformations
⢠anastomotic hemorrhage,
⢠Diverticulosis
71. ⢠The basic principles of management of postoperative GI bleeding
include the following:
1. Fluid resuscitation and restoration of intravascular volume
2. Checking and monitoring clotting parameters and correcting
abnormalities as needed
3. Identification and treatment of aggravating factors
4 Transfusion of blood products
5. Identification and treatment of the source of the bleeding
72. d) Stoma Complications
⢠Stomas are widely used in the treatment of colorectal, intestinal, and
urologic diseases.
⢠Can be early (<30 days) vs late
⢠Ischemic necrosis âa tight aperture
- overzealous trimming of mesentery, or
- mesenteric tension
retraction - tension on the bowel or
-ischemic necrosis of the stoma.
73. ⢠Late retraction - increased thickness of the abdominal wall with
weight gain.
⢠Stenosis âa small aperture, so-called natural maturation, ischemia,
-recurrence of Crohnâs disease, or carcinoma.
Mucocutaneous separation- ischemia,
- inadequate approximation of mucosa to
the dermal layer of skin,
- excessive bowel tension, or
- peristomal infection.
74. ⢠prolapse is most alarming to the patient and can result in incomplete
diversion of stool, interfere with the stoma appliance, lead to leakage
of stool, or become associated with obstructive symptoms and
incarceration.
⢠Parastomal hernia
⢠A peristomal fistula - Crohnâs disease,
- a deep suture used to mature the stoma, or
- may be caused by trauma from an appliance
75. ⢠Chemical dermatitis- manifested as erythema, ulceration (ileostomy
effluent), encrustation (urostomy effluent), or pseudoepitheliomatous
hyperplasia.
⢠Infectious dermatitis
⢠Allergic dermatitis
⢠Traumatic dermatitis
⢠diarrhea and dehydration.
⢠Psoriasis, Pyoderma gangrenos
⢠parastomal varices
76. Stoma Complications
CATEGORY EARLY LATE
Stoma Poor location
Retraction
Ischemic necrosis
Detachment
Abscess formation*
Opening wrong end
Prolapse
Stenosis
Parastomal hernia
Fistula formation
Gas
Odor
Peristomal skin Excoriation Dermatitis* Dermatoses
Parastomal varices
Cancer
Skin manifestations of
inflammatory bowel disease
Systemic High output Bowel obstruction
Nonclosure
77. Treatment
ď§ Prevention with sound surgical technique
ď§ Re laparotomy
ď§ Local revision
ď§ Revision of the stoma
78. e) Anastomotic Leak
⢠Anastomotic leak is a dreadful complication to encounter
⢠The level of the anastomosis in the GI tract is important.
⢠Although small bowel, ileocolic, and ileorectal anastomoses are considered
safe,
⢠Esophageal( lack of serosa)
⢠Pancreaticoenteric -the texture of the gland
- size of the pancreatic duct,
-the presence of pancreatic duct obstructive lesions
- experience of the operating surgeon
⢠Colorectal anastomoses -in the rectum, the highest leak rate is found in
anastomoses in the distal rectum, 6 to 8 cm from the anal verge.
79.
80. DIAGNOSIS
⢠The early warning signs of anastomotic leak are tachycardia, malaise,
fever, abdominal pain, ileus, localized erythema around the surgical
incision, and leukocytosis ,bowel obstruction , pneumaturia, fecaluria,
and pyuria.
⢠Sepsis is a prominent feature of anastomotic leakage and results from
diffuse peritonitis or localized abscess, abdominal wall infection, or
contamination of a sterile site with intestinal contents.
81. ďąprevention :
⢠Avoidance of anastomosis -In emergencies, immunocompromised,
nutritionally depleted patients and in the presence of fecal peritonitis,
significant bowel dilation, and edema,
⢠Mechanical and chemical bowel preparations
⢠Construction of an anastomosis requires :
1.Adequate exposure, gentle handling of tissues, aseptic precautions,
2.Adequate mobilization
3.Correct technical placement of sutures or staples
4.Matching of the lumens of the two organs
5.Preservation of blood supply to the ends
82. TREATMENT
⢠Resuscitation
⢠NPO and NG tube insertion
⢠Infected surgical wounds are opened, and
⢠Any abdominal wall abscesses are incised and drained.
⢠Reoperation is indicated if there is diffuse peritonitis, intra-abdominal
hemorrhage, suspected intestinal ischemia, major wound disruption,
or evisceration.
83. f)Intestinal fistula
ď§ Abnormal communication between two lining epithelium
Etiology:
1. Anastomotic leak
2. Poor blood supply
3. Trauma
4. Infection
5. Inadvertent suturing of bowel wall while closing the fascia
6. Carcinoma
ď§ Spontaneous closure in 40 to 80% of pts
84. ⢠Triad of manifestation
⢠sepsis,
⢠fluid and electrolyte imbalance,
⢠malnutrition
⢠Classified in to high and low output(<200, >500)
85. ⢠Treatment
⢠Prevention of occurrence
⢠Operation in 30 to 60%
⢠Resuscitation, TPN, correction of electrolyte
⢠Broad spectrum IV abcs
⢠H2 antagonist &PPI
⢠Nutrition (TPN, vitK, trace elements and multivitamin)
⢠Intra abdominal abscess drained
⢠Somatostatin analogue
⢠90% will heal within 4 to 6 weeks
86. RENAL AND URINARY TRACT COMPLICATIONS
⢠a)Urinary retention
⢠Inability to evacuate a urine-filled bladder
⢠It is a reversible abnormality resulting from disco-ordination of the trigone
and detrusor muscles as a result of increased pain and postoperative
discomfort
⢠Common in
⢠Perianal operation
⢠Hernia repair
⢠Rectal cancer
⢠Management
⢠Analgesics
⢠Judicious IV fluid administration
⢠Catheterization
87. b)Urinary Tract Infection
⢠Infection of the lower urinary tract is the most frequently acquired nosocomial
infection
⢠Principal contributing factors
⢠Preexisting contamination of the urinary tract
⢠Urinary retention
⢠Instrumentation
⢠In those patients who are catheterized for less then 48 hours, the risk of bacteriuria is about 5%
⢠Cystitis is manifested by dysuria and mild fever and
⢠pyelonephritis by high fever and flank tenderness
⢠Treatment includes
⢠Adequate hydration
⢠Proper drainage of the bladder
⢠Specific antibiotics
88. c) Acute renal failure
⢠is characterized by a sudden reduction in renal output that results in
the systemic accumulation of nitrogenous wastes.
⢠Hospital-acquired renal insufficiency adversely affects surgical
outcomes and is associated with significant mortality, especially when
dialysis is required.
⢠Oliguric Vs nonoliguric
89.
90. Diagnosis and managemnet
⢠ARF is diagnosed when there is a rise in serum creatinine, decrease in
creatinine clearance, and urine output less than 400 mL/day.
⢠Distinguishing between prerenal and renal azotemia is important.
⢠Anuria that suddenly develops postoperatively in an otherwise healthy
individual with no preexisting renal disease is postrenal in nature until
proved otherwise.
⢠Prevention requires identification of patients with preexisting renal
dysfunction; avoidance of hypovolemia, hypotension, and medications that
depress renal function; and judicious use of nephrotoxic drugs.
⢠Optimizing cardiac output and volume expansion
91. ⢠Treatment of ARF includes
⢠Management of fluid and electrolyte imbalance
⢠Careful monitoring of fluid administration
⢠Avoidance of nephrotoxic agents and adjustment of doses of renally excreted
medications until recovery of renal function
⢠Provision of adequate nutrition
⢠Most urgent in management of ARF is treating hyperkalemia and fluid
overload.
⢠When supportive measures fail, consideration must be given to
hemodialysis.
92. ENDOCRINE GLAND DYSFUNCTION
⢠a)Adrenal Insufficiency
⢠Adrenal insufficiency is an uncommon but potentially lethal condition
⢠failure of the adrenal glands to produce adequate glucocorticoids.
⢠Classified as acute and chronic adrenal insufficiency
⢠A) Acute adrenal insufficiency may occur as a result of abrupt
cessation of pharmacologic doses of chronic glucocorticoid therapy,
surgical excision or destruction of the adrenal gland (adrenal
hemorrhage, necrosis, or thrombosis in patients with sepsis or
antiphospholipid syndrome), or surgical excision or destruction
(postpartum necrosis) of the pituitary gland.
93. ⢠Present as unexplained hypotension or hemodynamic instability
develops despite fluid resuscitation, as well as ongoing evidence of
inflammation without an obvious source of infection. Hyponatremia is
usually present and does not respond to saline infusion, in severe
cases may lead to delirium, coma, and seizures. Hypoglycemia and
azotemia may also be present.
⢠An ECG will occasionally reveal low voltage and peaked T waves.
94. ⢠B)Chronic adrenal insufficiency - primary destruction of the adrenal gland
or be secondary to a disease state or disorder involving the hypothalamus
or anterior pituitary gland.
C/F -Nonspecific -fatigue, weakness, anorexia, weight loss, orthostatic
dizziness, abdominal pain, diarrhea, depression, hyponatremia,
hypoglycemia, eosinophilia, decreased libido and potency
⢠Primary hypoadrenalism also show manifestations of elevated plasma
levels of corticotropin &(hyperpigmentation of the skin and mucous
membrane).
⢠Patients with secondary disease, initially have neurologic or
ophthalmologic symptoms (headaches, visual disturbances) before
showing signs of HPA axis disease (hypopituitarism).
95. lab
⢠To diagnose the condition, cortisol and corticotropin concentrations
are checked and the rapid corticotropin stimulation test performed.
⢠The morning plasma cortisol concentration greater than 19 mg/dL
(525 nmol/L) rules out adrenal insufficiency and less than 3 mg/dL (83
nmol/L) indicates its presence.
⢠Supporting laboratory test abnormalities, including hyponatremia,
hyperkalemia, acidosis, hypoglycemia or hyperglycemia, normocytic
anemia, eosinophilia, and lymphocytosis, are present to a variable
extent
96. Treatment
⢠Patients receiving chronic corticosteroid therapy should be given adequate perioperative
corticosteroid administration.
⢠A stress dose of hydrocortisone (100 mg) may be given with induction of anesthesia.
⢠For minor surgical procedures, usual maintenance dose is continued postoperatively.
⢠For major surgical procedures, a stress dose (100 mg) is continued every 8 hours until
stable or free of complications and then tapered to the usual maintenance dose.
⢠Symptomatic patients are treated with hydrocortisone or cortisone.
⢠Patients who have received more than 20 mg of prednisone daily for more than 3 weeks
within the previous year and
⢠patients with Cushing's syndrome who are undergoing surgery are presumed to have
HPA suppression and must be treated in a similar fashion.
97. b)Hyperthyroid Crisis
⢠Thyroid crisis is a medical emergency that occurs in thyrotoxic
patients, frequently precipitated by a stressful event and
characterized by exacerbation of hyperthyroidism and
decompensation of one or more organ systems.
⢠Mortality is high, ranging from 20% to 50% if the crisis is
unrecognized and left untreated
⢠Clinical manifestations of hyperthyroidism include nervousness,
fatigue, palpitations, heat intolerance, weight loss, atrial fibrillation
(in the elderly), and ophthalmopathy characterized by eyelid
retraction or lag, periorbital edema, and proptosis.
98. ďśThe onset of thyroid crisis is sudden and characterized by accentuation of
the symptoms and signs of thyrotoxicosis and organ system dysfunction, including
⢠hyperpyrexia, tachycardia out of proportion to fever, dehydration and collapse,
⢠central nervous system dysfunction (delirium, psychosis, seizure, coma),
⢠cardiac manifestations,
⢠GI symptoms, and liver dysfunction.
ďśIx
-Elevated (Free thyroxin (T4) and triiodothyronine (T3) ) and
suppressed (TSH) levels
-Thyroid scintigraphy)
99. Treatment
⢠Identification and treatment of the precipitating factor
⢠Supportive care - Oxygen, Intravenous fluid therapy, Sedation
(chlorpromazine) , Venous thromboembolism prophylaxis with
heparin, Dexamethasone, antipyretics and cooling, Heart failure:
digoxin and diuretics, Atrial fibrillation: intravenous heparin
⢠Specific medications (iodine, propylthiouracil, β-adrenergic blockers,
dexamethasone), Plasmapheresis and charcoal plasma perfusion or
exchange transfusion if no response in 24-48 hours
⢠Once euthyroidism is achieved, definitive therapy must be considered
to prevent a second crisis
100. c)Hypothyroidism
⢠Occur in patients with preexisting chronic hypothyroidism
⢠Exacerbated as a result of severe stress, like surgery, severe illness,
physiologic stress, and drugs that inhibit peripheral conversion of T4
to T3.
⢠Hypothyroidism may be primary (surgical removal, ablation, or
disease of the thyroid gland), secondary (hypopituitarism), or tertiary
(hypothalamic disease).
101. Clinical manifestation
⢠Chronic hypothyroidism can be asymptomatic or demonstrate cold
intolerance, constipation, brittle hair, dry skin, sluggishness, weight
gain, and fatigue.
⢠The impact of hypothyroidism is greatest on the cardiovascular
system ( bradycardia, hypotension, impaired cardiac function,
conduction abnormalities, pericardial effusion, and increased risk for
CAD). Also, worsening of pulmonary function, a predisposition to
pleural effusion, and susceptibility to hypothermia.
⢠Rarely have the severe form (myxedema coma) characterized by
coma, loss of deep tendon reflexes, cardiopulmonary collapse, and
high (âź40%-50%) mortality
102. lab
⢠In primary hypothyroidism - serum total T4, free T4, and free T3 levels
are low, whereas TSH is elevated.
⢠In secondary disease, TSH, the free T4 index, and free T3 are low.
Distinguishing the two is important because adrenal insufficiency is
present in secondary disease and administration of levothyroxine
must be accompanied by cortisol or the disease could be
exacerbated.
⢠On in ECG - bradycardia, low voltage, and prolonged PR, QRS, and QT
intervals
103. Treatment
⢠In patients with symptomatic chronic hypothyroidism, surgery is
postponed until a euthyroid state is achieved.
⢠Postoperatively, if patients shows clinical signs of significant
hypothyroidism (severe postoperative hypothermia, hypotension,
hypoventilation, psychosis, and obtundation) are immediately treated
with thyroid hormone, concomitant with the IV administration of
hydrocortisone, to avoid an addisonian crisis.
104. Neurologic complication
⢠A)Delirium
refers to a state of acute confusion and is a common complication
of surgery.
⢠Causes
⢠Post operative anemia(secondary to acute blood loss)
⢠Electrolyte imbalance
⢠Sepsis
⢠Malnutrition physical restraints
⢠Extended duration of anesthesia ,respiratory complication
⢠Infection
105. ⢠Delirium tremens the most common threatening disorder occurs 48
hrs to 14days after alcohol withdrawal
⢠Tremor,
⢠fever,
⢠confusion,
⢠tachycardia,
⢠psychosis,
⢠agitation and seizure
106. ⢠Treatment
⢠Identification and elimination of precipitating factor
⢠Treatment of associated laboratory abnormality
⢠Cxr and u/a for source of infection
⢠ECG for evidence of MI
⢠Haloperidol 0.5 to 2mg
⢠benzodiazepine
⢠Beta blockers(autonomic manifestation)
⢠Clonidine(HTN)
107. b)Seizure disorders
⢠Risk factors
⢠Hx of epilepsy
⢠Alcohol withdrawal
⢠Antidepressants
⢠Hypoglycemic agents
⢠Lidocaine
⢠Presentation
⢠Convulsions, rhythmic myoclonic activity, loc often associated with fecal and urinary
incontinence, lack of neurologic responsiveness, and postevent amnesia
⢠Treatment
⢠Benzodiazepines ,phenytoin ,carbamazepine ,valproic acid
108. c)Stroke and TIA
⢠A stroke in the perioperative period has devastating outcome.
⢠Strokes are more commonly associated with cardiovascular procedures.
⢠Hemorrhagic strokes are uncommon, and their effect can be more
devastating than ischemic strokes.
⢠Prevention of a perioperative stroke starts with the identification of at-risk
patients.
⢠Patients with hypertension must receive adequate treatment, and
overzealous correction must be avoided.
⢠Patients with atrial fibrillation benefit from prophylaxis with
anticoagulants.
⢠Patients with a carotid bruit must be evaluated with noninvasive vascular
studies and treated accordingly.
109. ⢠Patients undergoing a high-risk surgical procedure (e.g., Carotid
endarterectomy) may be monitored
⢠Adequate hydration and monitoring in the perioperative period to
avoid hypotension and fluctuations in blood pressure.
⢠A diagnostic workup is started immediately to distinguish between
hemorrhagic and ischemic stroke with a ct scan.
⢠Further tests depend on the clinical scenario: an echocardiogram , a
carotid duplex scan ,a cerebral angiogram and others.
⢠Treat according based on the type of stroke and underlying factor
110. Prophylactic & therapeutic antibiotics
⢠Prophylactic antibiotics are used most often to prevent infection of a
surgical incision
⢠Antibiotic prophylaxis is indicated for most clean-contaminated and
contaminated (or potentially contaminated) operations.
⢠An example of a clean-contaminated operation in which antibiotic
prophylaxis is usually not indicated is elective laparoscopic
cholecystectomy.
⢠antibiotic prophylaxis is indicated for high-risk biliary surgery( age> 70
years, diabetes mellitus, or a recently instrumented biliary tract (e.g,
Biliary stent& colorectal surgery)
111. ⢠Antibiotic prophylaxis of clean surgery is controversial.
⢠When bone is incised (e.g., craniotomy, sternotomy) or a prosthesis is
inserted, antibiotic prophylaxis is generally indicated.
⢠Some controversy persists with clean surgery of soft tissues (e.g.,
breast, hernia).
⢠principles antimicrobial agent for prophylaxis:
1. Safety
2. An appropriate narrow spectrum of coverage of relevant pathogens
3. Little or no reliance on the agent for therapy of infection (because of
the induction of resistance with heavy use)
112. 4. Administration within 1 hour before surgery and for a defined brief
period thereafter (no longer than 24 hours, 48 h for cardiac surgery)
o Antibiotics given sooner are ineffective, as are agents given after the
incision is closed.
oAntibiotics with short half-lives (t1/2 < 2 hours; e.g., cefazolin or
cefoxitin) should be re dosed every 3 to 4 hours during surgery if the
operation is prolonged or bloody
ďąTherapeutic antibiotics âdirty wounds, suspect infection