Preoperative assessment of surgical patient

1- Assessment

History:
- C. V.S: anemia - HTN - IHD.
- Respiratory: Infection (Should be treated 1st) - asthmatic – COPD.
- GIT: Peptic ulcer & GERD
- Genitourinary: UTI
- Endocrinal: D.M (Control before operation)
- Infectious disease: HIV - HCV – HBV - T.B.
- Drug History: Allergy – Addiction.
- Previous Surgery: type of anesthesia & presence of complications

Physical examination:
- General examination
- Cardiovascular examination
- Respiratory
- Gastro-Intestinal
- Neurological.
- Genitourinary
- Specific Surgical Site examination.

Investigations:-
 Routine Labs:
- CBC- BL Sugar level - Urine Analysis
- Coagulation profile.
- ABG, PH, Electrolyte
- Renal & Liver functions.

 Cardiovascular: - E.C.G +- Echo

 Respiratory: - Chest X Ray. - Screening for long Tumors.

1
 2- Preoperative preparation

[1] Consent: must be signed before the operation.

[2] Preoperative round:
- Final reexamination of patient. - mark the side to be operated.
- Assure investigation are Completed.
- prepare Blood if transfusion required

[3] Diet
- Day before operation: High Caloric diet.
- Fasting 6-8h before time of operation

[4] Bowel preparation:

- Purgative. – Enema. - NGT (Before GIT procedures)

[5] Skin preparation:

- Shaving. - Shower with 10% povidine iodine.

[6] Maintenance of fluid Balance:

- IV fluids. - Urinary Catheter to monitor output.

[7] Pre anesthetic Medication

- Sedation: Benzodiazepine - opioids
- Cardiac: Anti HTN drugs. Labetalol in urgent surgery
- Gastric acidity: H₂ Blocker – P.P inhibitors.

 Medication to be continued
- CVS medications: - Ca channel Blocker - Beta Blockers
- Anti-arrhythmic - nitrates. - Aspirin
- Bronchodilators withdrawal Cause Bronchospasm.
- Antiepileptic.
- Steroid: sudden stop causes addisonian crisis

 Medication to be stopped. D
- Warfarin: stopped 4 days before operation
- Contraceptive Bills.
- MAO inhibitors.
- SSR Inhibitors.
2
 Wound Healing

Factors affecting wound healing:

 General Factors
1- Age: Wound healing is slow in elderly persons due to a reduced rate of
protein turnover.
2- Nutritional states
- Protein deficiency → ↓ collagen synthesis.
- Vitamin C deficiency → lack of maturation of protocollagen.
- Vitamin A deficiency → deficient epithelialization.
- Ca, zinc, Cu & Mg also affect wound healing.
3- Debilitating diseases:
- Uremia, jaundice, cirrhosis,
- DM & malignancy delay wound healing.
4- Drugs:
- Steroids and cancer chemotherapy & immunosuppressive drugs impair
wound healing.

 Local factors:
1- Vascularity: A good blood supply (e.g. in the face &scalp) → nice healing
while a poor blood supply (wounds below the knee) → delayed healing.
2- Immobilization: Movement damages the bl. supply → delayed healing.
3- Irradiation: endarteritis obliterans → Ischemia →↓ wound contraction &
granulation tissue format.
4- Tension: ↑↑ tension e.g. (sutures under tension, hematoma, and
infection) → ischemia & impaired healing.
5- Infection: Fibroblasts compete with bacteria for oxygen & nutrition,
bacteria secrete collagenolytic enzymes, which destroy collagen fibers.
6- FBs & necrotic tissue: impair wound healing.
7- Adhesion of wound to a bony surface: Prevents wound contraction e.g.
chronic venous ulcers.
8- Impaired venous drainage: as in postphlebitic limbs impairs wound
healing.

3
 Complications of wound healing

1. Wound failure (wound dehiscence):

- Failure of an abdominal wound is called burst abdomen.

2. Stretching of the scar.

3. Hypertrophic scar:
4. Keloid:
- Definition: overactivity of the healing process → excessive scar tissue.
- Course: Progressive even after 6 months.
- Sites: Ear lobules, shoulder, presternal area.
- Incidence: Black persons are more prone to keloid formation and there is a
familial predisposition.
- TTT of hypertrophic scars & keloids:
a. Continuous pressure by silicone gel sheets.
b. Intralesional corticosteroids.
c. Surgical excision: Recurrence rate after simple excision may reach 80%.
To minimize recurrence intramarginal excision of the scar + intraoperative
injection of steroids are recommended.

5. Contracture:
- Pathological shortening of scar tissue→ deformity if the scar overlies a
joint.

6. SSI.

4
 BURN
Definition: necrosis of tissue by physical or chemical agent

Cause:
- Physical: thermal (75%) - electrical - Radiation
- Chemical: Acids / Alkalis

Classification:
 Acc. to extend:
- major Burn: > 30% of body surface
- intermediate: 15-30% in adult
10-30% in children.
- minor: ↓ 15% in adult
↓10% in Childress
-
 Acc. to depth:
- 1st degree: epidermis only.
- 2nd degrees: epidermis + part of Dermis
- 3rd degree: epidermis + Dermis
-

Complication: (1ry Cause of Death in Burn is infection)

[A] Systemic
- Inhalation injury: early: asphyxia
Late Bronchospasm.
Finally Resp. Failure Type II

- Shock: Hypovolemic, neurogenic, septic

- Renal: oliguria - electrolyte imbalance
- GIT: acute gastric dilatation - ulcers - paralytic ileus - Hepatic Dysfunction
- Endocrinal: ↑ Cortisol & ADH - ↑ protein Catabolism. - ↑ Adrenaline.
- CVS: ↓ COP & HF
- Psychological: anxiety, irritability, depression
- Multi organ Failure
5
 [B] Local Complications:

- [1] Infection: within 7 days, TTT by proper Burn wound Care

- [2] Constricting Escher.
- [3] Compartment $
- [2] Joint Contracture
- [5] Scar Formation
- [6] Malignant transformation: Marjoline ulcer

C/P:
- Pain: sever in superficial & less in deep.
- local tissue edema
- features of Complications

TTT:
A- 1st TTT:
• Move & remove: move patient from source of Burn - remove all clothes.
- Airway maintained
- Breathing maintained
- Circulation maintained
- analgesic (morphine) & anti tetanic
- Run water at room Temperature
B- Definitive TTT:
 Minor Burn
- Treated as outpatient: clean & Betadine or Savlon
Dressing by sulfadiazine – Vaseline gauze
Analgesics, prophylactic AB
 Major Burn
- Hospital admission at Burn unit.
- resuscitation & monitoring: - Wide Broad Cannula - CV Line
- Foley Catheter urine output monitoring
- Ryle tube
- NPO For 48h then oral Feeding
- Vital signs monitoring
6
 - Fluid therapy:
- Time: in the 1st 48h. Then acc. to patient response
- Formula: Evan’s Formula

- 1st day:
1 ml/Kg/ %.Burn ………………… Normal saline
1 ml /kg/ %Burn ………………… Colloid
2000ml…………………………....... Glucose

- 2nd day:
0.5 ml/Kg/ %.Burn …………….. Normal saline
0.5 ml/Kg/ %.Burn……………… Colloid
2000 ml …………………………….. Glucose

• Monitory of adequate intravenous resuscitation by urine output vital signs

- Local Burn wound Care:

- Escharotomy in Constricting Escher in limb / chest.
- Fasciotomy in Deep Burn
- removing loose skin & tissue Debridement
- Topical antimicrobial

Then either:
- Exposure methods leaving the wound exposed under aseptic precaution
- Covering the wound by Bulky dressing, changed every 2-3 Days.

7
 Hypokalemia Hyperkalemia
Definition ↓ serum K <3,5 mmol/L ↑ serum K > 5.3 mmol/L.
N = (3.5 – 5.3 mmol/L)

Causes ↓ Intake: Starvation ↑ Intake: over correction.

↓Absorption: malabsorption $ ↑ cellular release:
↑ intracellular: - Hemolysis
- insulin therapy - Rhabdomyolysis
- Alkalosis - Metabolic acidosis
↑ renal Loss: - Insulin deficiency
- Diuretics (loop_ - Digitalis toxicity
Thiazide) - Tumor Lysis $
↑ GIT loss: ↓ Excretion: renal failure
- vomiting - suction
Hazards ↓ Nerve & muscle excitability.
↑ Risk of arrhythmia (in patient
taking Digoxin)
↑ Risk of hepatic Coma in
patient è liver disease.
polyuria → ↓ response to Anti
Diuretic hormone
C/P: - Asymptomatic - Skeletal Muscle weakness up
- Skeletal muscle weakness to paralysis.
up to paralysis. - Cardiac: ↓ HR - ↓ BL.P.
- Cardiac: arrhythmia - GIT: Constipation
- GIT: Constipation up to - CNS: confusion
paralytic ileus.
- Glucose intolerance
- Features of the Cause
Investigation - PH: Alkalosis - PH: Acidosis
- serum K Level: Decreased - serum K Level: increased
- Urinary K level. - Urinary K level.
- ECG changes - ECG changes
- investigation of the Cause - investigation of the Cause

8
TTT  Treatment of the Cause  Treatment of the Cause
 Hyperkalemia correction:
 potassium replacement:
↓ 7 mmol/L:
- Oral K: in mild cases. - IV NA Bicarbonate.
- IV K: Slowly - Glucose 25% + 20 unit
in large vein insulin over 3H
under ECG monitoring
↑ 7 mmol/L:
- Dialysis.

 Ca Gluconate

9
 Hypocalcemia
Causes:
 decreased PTH that can be caused by:
- hypoparathyroidism - pseudo-hypoparathyroidism
- renal osteodystrophy
 decreased Vit D3

Presentation
 Symptoms of hypocalcemia:
- Fingertip, toes, perioral. - abdominal pain & biliary colic
- muscle (cramp & tetany) - convulsions
- dyspnea (laryngospasm. bronchospasm)
- Mental status changes: anxiety, fatigue, mood swings.
 Dermatological:
- fungal nail infections - hair loss
- Blotchy skin: pigment loss, vitiligo.

 findings of tetany
- Trousseau's Sign
- carpopedal spam after inflating BP cuff 20mmHg above systolic BP x
3-5min
- MCP flexed, DIP and PIP extended position
- more sensitive than Chvostek's sign
- Chvostek's sign:
- Facial muscle contractions after tapping on the facial nerve.

Investigations:
- Serum Ca. phosphate. Vit D , PTH
- Serum albumin: low
- PH: Alkalosis ↑ albumin binding to ionized calcium → hypocalcemia.
- ECG: prolonged QT interval

TTT:
- Ca gluconate infusion (with cardiac monitoring to prevent hypercalcemia).
- Activated Vit D3

10
 Hyperparathyroidism
Causes:
 1ry Hyperparathyroidism (The Commonest)
- Single adenoma 85%. - multiple adenoma
- Hyperplasia - Carcinoma

 2ry Hyperparathyroidism:
- ↓ Ca: malabsorption $ - Chronic renal failure.

 3ry Hyperparathyroidism:
- chronic kidney disease
- Usually after longstanding secondary hyperparathyroidism.

Clinical presentation
 Bone: - osteitis fibrosa cystic - Bone aches - Pathological #.
 Articular: Chondrocalcinosis (Ca deposition in articular Cartilage)
 Renal stones: Hyper Calciuria & phosphaturia causing recurrent renal
stones.
 Abdomen: ↑ Gastric, pancreatic secretion 2ry to → hypercalcemia →
Peptic ulcer, pancreatitis.
 Psychic moans: irritability, personality changes, even neurosis.
 Hyperparathyroidism crisis:
- muscle Weakness - weight loss
- Nausea & vomiting - Fatigue & Drowsing.

Investigations:
 labs
- ↑ Serum Ca - ↑ excretion of Ca in urine - ↑ plasma level of PTH

 Imaging (X-Ray):
- skull: Salt & pepper appearance
- Hand: subperiosteal resorption
- long Bone: osteitis fibrosa cystic

 Thyroid: - U/S - CT scan - Tc scan.

11
Treatment
- If single adenoma: excision & exposure of other glands to ensure are of
normal size and take sample.

- If Hyperplasia: - subtotal parathyroidectomy.

- Total parathyroidectomy with Transplantation of very
thin slices in Forearm muscle.

12
 D.D. of unilateral limb swelling

 Trauma:
- # Dislocation.
- Lig injury
- plantaris rupture
- Backer cyst rupture
- Calf muscle contusion.

 Infection:
- Cellulitis
- Gas gangrene
- Necrotizing Fasciitis

 vascular
- DVT
- Varicose veins.
- AV Fistula wat
- Compartment $

 Lymphatic:
- lymphatic obstruction
- Lymphatic edema.

13
 Acid Base Balance

• Normal pH (7.4 +- 0.4)

- Renal regulation → H₂C03 Reabsorption & H+ excretion.
- Resp. regulation → Co₂ elimination

Metabolic acidosis
Definition:
- Condition of Base deficit & acid excess rather than H₂C03.

Causes
 ↑ H+ Formation
- DM & DKA
- Lactic acidosis (sepsis, Shock).
- Starvation

 ↓ H+ excretion:
- Renal failure (acute & chronic).

 loss of H₂C03:
- Diarrhea
- uretero-sigmoid anastomosis

C/P:
- Air Hunger (Rapid, shallow)
- Nausea 2 vomiting Drowsiness

TTT:
- Treat the cause.
- IV H₂C03 in severe cases.

14
 Metabolic alkalosis
Definition:
- Condition of Base excess or acid deficit.

Causes
- Loss of gastric HCL: vomiting, aspiration, antacids.
- Cushing $
- Conn's $
- Mills alkali $

Clinical Picture
- Cheyne stroke respiration (slow, deep) with attacks of apnea
- Tetany: ↓ ca

TTT
 Mild Case:
No hypokalemia→ IV NaCL.
Hypokalemia → IV KCL

 Sever Cases:
IV ammonium chloride & Hydrogen chloride very slowly

 If Tetany:
IV Calcium gluconate.

15
 Respiratory acidosis Respiratory alkalosis
Causes  Respiratory depression:  ↑ resp. rate:
- CNS lesion. - Hysterical
- Cardiac arrest - Hyperpyrexia
- Drugs as opiate
 Brain stem lesion
 Respiratory:  Bacterial Sepsis
- Muscles Disorder: Myasthenia.
- obesity
- Pulmonary edema.
- COPD
C/P: Restless - Tetany in severe
cyanoses
alkalosis.
↑HR
- respiratory arrest
↑RR
HTN
TTT improve ventilation: O2 mask & Breathing in a bag
mechanical ventilation

16
 Post-operative Fever

Causes:
 First 24H:
- Normal response
- Pre-existing infection
- Transfusion reaction.
- Addison crisis.
- Thyroid storm
- Drug fever.

 1-7 Days:
- Wind (Resp. problem) → pneumonia
- Water: UTI
- Wound: surgical site infection
- Wonder drug: drug fever
- Withdrawal: Alcohol
- Walking: venous thrombo-embolism

 1-4 week:
- Abscess
- Drug Fever
- Central line infection.

 Delayed > 1 m
- Infection (viral, Bacterial, fungal)

Implant infection ‫وتكمل زى ال‬

17
 Wound & Hardware infection

Risk Factors:
- Extremity of ages.
- Immunosuppressive drugs “Steroids"
- Bad general conditions.
- Systemic diseases that impairs host defense.
- Length of Hospital Stay!

Mechanism: (pathology)
 Seeding:
- Disruption of soft tissue envelope, BL.V & periosteum: Allow Bacteria to
avoid host defense
- Direct Seeding of implant and / or anatomical structure.
- Haematogenous seedling
 Biofilm Formation:
- By Bacteria on implant within 4 weeks
- 15% cell + 85%, Glycocalyx.
- Eradication is difficult so removal is essential.

Presentation
 History:
- Extend of soft tissue injury.
- Extend of bony injury.
- previous or current Hardware
- previous or current surgery at the same side
- Previous skin or deep infection.
 Symptoms
- pain at previous fracture site may indicate infected nonunion
- Fever, chills, night, night sweating.

Examination:
- Erythema, Drainage or purulence. - Tenderness. – ROM.

18
Imaging
 X-Ray: Biplanar Imaging of affected site.
- Findings:
- Acute infection: May be normal.
- Subacute & chronic infection.
- peri-implant radiolucency
- Involucurum: reactive Bone Surround active infection
- Sequestrum: infected Necrotic Bone
 CT scan: Preoperative planning.
 MRI: Extend of Lesion. - Soft tissue mass - fluid collection.
 WBC labeled scan
- Differentiate infection from other similar etiologies.

Labs:
- WBC may be normal in chrome infection.
- ESR
- CRP: most predictive for postoperative infection
 Culture:
- Culture swab (or) aspiration of wound: Not reliable.
- Intraoperative deep culture: The most reliable.

TTT:
 Conservative:
- supportive measure
- AB: empirical then acc. to C&S. I.V then Oral.

 Operative
- Like Surgical Debridement & Drainage
- removal of implant
- Wound AB (vancomycin powder).
- Drilling of bone to evacuate any pus present.
- shingling of bone ends ↑ vascularity
- closure over AB Beads or VAC
- 2ry lock may be needed
- Avoid Drain … ↑ risk of infection
- Post-operative IV AB.
19
 Post-operative infection
As implant infection But:

Source of infection
 intra operative:
- air, gowns, gloves - Surgeons - Instruments
 post-operative:
- Drains - Haematogenous

Classification
 acc. to extend •
- Superficial infection: skin subcutaneous tissue + No fascia
- Deep infection: involve fascia and /or muscle
 acc. to onset
- Acute (< 3W)
- Chronic (3W - 12m).
- Late (> 12W) related to haematogenous infection from another focus.

Prevention:
 Pre-operative:
- Shaving – late admission – TTT of any septic focus
 Intra operative
- small Team - UVR (Bactericidal)
- Vertical ventilation system.
- Head, feet wear, gowns, gloves & face mask.
- instrument sterilization - Field sterilization
- Proper soft tissue handling
- avoid along operation time
- Avoid drains: ↑ risk of infection.
 Post. Operative:
- AB. Therapy.
- Follow up the wound è frequent dressing.

20
 Nosocomial infection
Causes:
 Organism
- Bacteria: staph. & strept
- Viruses HIV,HBV, HCV, influenza,
- Fungal: as Candida

 Predisposing factors:
- Extremity of ages. - Bad general conditions
- Immuno-Suppressive drugs: Steroids.
- Length of Hospital Stay. - Malnutrition
- Systemic diseases that impairs host defense.

 route of infection:
- Direct Contact. - Droplet
- Blood Born infection. - AIR born.

 Source of infection:
- Patient themselves. - visitors
- Medical staff - The hospital

 Types of infection:
- Respiratory: Pneumonia & TB.
- CNS. - GIT infection.
- UTI. - surgical site infection

Diagnosis:
- FAHM
- localized inflammation
- redness, Hotness, swelling, Tenderness

(Labs)
- TLC, ESR, CRP. ASOT
- IFAT IHAT, TB skin Test
- Blood culture.
21
Prevention: (TTT mainly prevention)

- Medical staff education about infection Control principles.

- Medical staff vaccinations.
- Medical staff personal protection (gloves, gown, masks).
- Frequent Hand wash.
- Surgical Technique (proper soft tissue Handling- proper hemostasis)
- Isolation of highly contagious pt. as TB.
- Isolation of High risk pt. (Burn- immune-compromised).
- Care of patient equipment’s (avoid reusing for another patient)
- Avoid prolonged Hospital stay & avoid needle prick.

22
 Necrotizing Fasciitis
Definition:
A life-threatening bacterial soft tissue infection that spreads along soft tissue
planes rapidly.

Risk factors
 immune suppression
- diabetes - AIDS - cancer - obesity
 bacterial introduction
- IV drug use. - insect bites - skin abrasions
- hypodermic therapeutic injections
- abdominal and perineal surgery

Associated conditions
- Cellulitis & abscess may be present.

PROGNOSIS
- Life threatening infection (mortality rate of 30%)
- mortality correlates with time to surgical intervention

CLASSIFICATION:

Type Organism Characteristics

Most common (80-90%)
Type 1 immunosuppressed (DM & cancer patients)
Polymicrobial
Postop abdominal and perineal
infections
Monomicrobial 5% of cases
Type 2 Group A β- Seen in healthy patients
hemolytic Extremities

Type 3 (gram negative

Marine exposure
rods)
Type 4 MRSA

23
PRESENTATION
Symptoms:
 early
- localized abscess or cellulitis with rapid progression
- minimal swelling - no trauma or discoloration
 late findings
- severe pain - high fever, chills and rigors
- tachycardia

Signs
- skin bullae - discoloration
- ischemic patches - cutaneous gangrene
- swelling, edema
- dermal induration and erythema
- subcutaneous emphysema (gas producing organisms)

IMAGING
- X-ray: not required for diagnosis or treatment.
- May help in DD with gas gangrene
- Biopsy: emergent frozen section can confirm diagnosis in early cases

TREATMENT
 Operative
- emergency radical debridement with IV antibiotics +- Fasciotomy

- amputation

24
 Gas Gangrene
(Clostridial myonecrosis)

ETIOLOGY:
 Organism:
- Clostridium perfringens (most common)
- found in soil and gut flora
 Pathophysiology
- gram-positive obligate anaerobic spore-forming rods that
produce exotoxins, causes muscle necrosis and vessel thrombosis, can
cause hemolysis and shock
- incubation period <24h
- Gas produced by fermentation of glucose.

Anatomic location
- buttocks, thigh, perineum

Risk factors
 posttraumatic (associated with C perfringens)
- car accidents (most common) - crush injuries
- gunshot wounds with foreign bodies - burns and frostbite
- IV drug abuse
 postoperative
- bowel resection or perforation - biliary surgery
- premature wound closure
 spontaneous
- colon cancer - neutropenia

PRESENTATION
 History
- recent surgery to GI or biliary tract
 Symptoms
- Triad:
- sudden progressive pain out of proportion to injury (from thrombotic
occlusion of large vessels)
- tachycardia not explained by fever
25
 - feeling of impending doom
 Physical exam
- sweet smelling odor - "dishwater pus" discharge
- Swelling, edema, discoloration and ecchymosis.
- blebs and hemorrhagic bullae - crepitus
- altered mental status

IMAGING
 X-Ray: linear streaks of gas in soft tissues

Labs
- LDH: ↑ - WBC: ↑
- Metabolic acidosis and renal failure.
- Culture: blood culture rarely grows Clostridial species

Histology
- Gram stain: Gram-positive bacilli
- absence of neutrophils

TREATMENT
 Nonoperative
- high dose IV antibiotics
- 1st line is penicillin G and clindamycin
- hyperbaric O2
 Operative: (1st line treatment is surgical)
- Radical surgical debridement with fasciotomies.
- Amputation: if irreparable diffuse myositis.

26
 Hand infection
- Due to use of Hand & it's exposure to Contamination (Frequency of Hand.
infection is High)

Classification:
1- Cutaneous, SC infection:
- Paronychia - pulp space infection
- web space infection
2- Fascial space infection:
- thenar space infection - Hypothenar space infection
- Mid palmar space infection.
3- synovial sheath infection
- Acute Digital teno-synovitis.
- ulnar Bursitis - Radial Bursitis
4- Bone & joint infection.

PRESENTATION
- History: manual worker with history of prick.
- FAHM
- Redness, hotness, swelling tenderness.
- The Fingers can't be approximated (Adduction)

Investigations:
- X-ray: if suspected of F.B & #.
- Blood sugar level to For those è recurrent infection

Treatment:
- Early administration of strong IV AB.
- Early Drainage of infection (don't wait for fluctuation.
- Debridement of all infected tissue under general anesthesia
- Incision: never cross Hand Crease.
- Use tourniquet (Bloodless field).
- Early ROM to avoid stiffness.
27
 Complications of Fractures
General Complications
- Shock: (hemorrhagic, neurogenic & septic).
- Fat embolism (young patient with hx of long bone # then on 2nd day: dyspnea,
drowsiness & petechial hemorrhage)
- Complications of prolonged recumbancy:
a. DVT & pulmonary embolism.
b. Bed sores, osteoporosis & constipation.
- Crush syndrome: acute renal failure.
- Infections: e.g. tetanus and gas gangrene

Local Complications
1- Skin: A- Injury. B- Infection. C- Sores.
2- Muscles & Tendons: A- Injury. B- Myositis ossificans
3- Blood Vessels:
A-Acute Ischemia (Arterial Injury).
Types: spasm, contusion, partial tear, complete tear.
Clinical picture: 6Ps (Pain. Pallor, Progressive coldness. Pulseless.
Paralysis & Paresthesia).
Treatment: reduction of the fracture:
If pulse returns: follow up.
If no pulse (within 20 minutes): Explore & repair it according to the type of injury.

B-Compartmental Syndrome C-Crush Syndrome.

D-Volkmann's Ischemic Contracture

4- Nerve Injury:
- Neuropraxia, axontemsis or neurontemesis.
- Treatment:

A- Closed: expectant Treatment For 6 weeks (massage + electric Stimulation)

If failed: explore & repair.

b- Open: mark the nerve at 1st then delayed suturing (no 1ry repair).

28
5- Joints:
A- Sudeck's Atrophy B- Myositis Ossificans

6- Bone
A-Non-union B- Delayed Union C-Malunion
D-Ischemic Necrosis (AVN).

29
 Post-Op IO
PARALYTIC ILEUS

1- Adynamic: paralytic ileus

DEFINITION:
- Paralysis of peristaltic activity of the gut.

Causes:
 Reflex inhibition of:
- intestinal motility following abdominal surgery or spinal # (sympathetic
overtone)
 Toxic inhibition of intestinal motility (peritonitis)
 Electrolytes Disturbance: ↓ K & NA
 Drug overdose: Anticholinergics

PRESENTATION
- Distension, Constipation, vomiting
- silent abdomen (No abdominal Colic)

Investigation:
- X-ray: Multiple Fluid gas level.
- Labs: K & NA.

Prevention:
- Pre-operative: Correction of Biochemical disturbance.
- Operative: gentle handling of intestines.
- Post-operative: Nasogastric tube to decompress The Bowel until return of
intestine Sound or passage of flatus

Treatment
- Gastrointestinal suction: Till intestinal Sound return.
- Iv fluids: K & NA
- Drugs: para-sympathomimetic: ex. prostigmine

30
 2- Dynamic:

Causes:
 Accidental suturing of gut during closure of peritoneum
 Early post-operative adhesion.

Diagnosis:
- as IO

TTT:
- Usually medical.

31