Surgical infection and Nutrition

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Infection and Nutritionin the Surgical Patients

Nyra E. MonteraSenior Clerk

Oct. 2011



INFECTION

Invasion of the body by pathogenic

microorganisms and reaction of thehost to organisms and their toxins



SURGICAL INFECTIONS

• A surgical infection is an

infection which requires surgical

treatment and has developedbefore, or as a complication ofsurgical treatment.



Clinical features

• Local- pain, heat, redness, swelling, loss of function

(apparent in superficial infections)

• Systemic- fever, tachycardia, chills

• Investigations:

Leukocytosis

Exudates- Gram stain, culture

Blood culture ( chills & fever )

Special investigations ( radiology, biopsy )



Factors contributing to infections

• Adequate dose of microorganisms

• Virulence of microorganisms

• Suitable environment ( closed space )

• Susceptible host



Principles of Surgical Treatment

• Debridement- necrotic, injured tissue

• Drainage- abscess, infected fluid

•

Removal- infection source, foreign body• Supportive measures:

• immobilization

• elevation• antibiotics



Pathogenesis of Infection



Host Defenses

• Entry of microbes into the host isprecluded by the presence of anumber of barriers that possess either

an epithelial (integument) or mucosal(respiratory, gut, and urogenital)surface.

• Host barrier cells may secretesubstances that limit microbialproliferation or prevent invasion.



• outcomes of microbial invasion and

the interaction of microbes withresident and recruited host defenses:

•

(a) eradication• (b) containment

• (c) locoregional infection

• (d) systemic infection



• Infection — defined by identification ofmicroorganisms in host tissue or thebloodstream, plus an inflammatory

response to their presence.

– At the site of infection, the classic findings

of rubor, calor, and dolor in areas such as

the skin or subcutaneous tissue arecommon.



• SIRS — characterized by a

sequence of host phenotypic andmetabolic responses to systemic

inflammation that includes

changes in heart rate, respiratoryrate, blood pressure, temperature

regulation, and immune cell

activation.



Microbiology of Infectious

Agents



Bacteria• Bacteria are responsible for the majority

of surgical infections.• Gram-positive bacteria:

– SSI-aerobic skin commensals(Staphylococcus aureus and epidermidis andStreptococcus pyogenes) and entericorganisms such as E. faecalis and faecium.

– enterococci can cause nosocomialinfections (UTIs and bacteremia) inimmunocompromised or chronically illpatients

• gram-negative organisms – Enterobacteriaceae spp, and Pseudomonas

spp



STREPTOCOCCI

• Gram positive

• Flora of the mouth and pharynx, (bowel)

• Streptococcus pyogenes – ( β hemolytic) 90% of

infections e.g.,lymphangitis, cellulitis, rheumaticfever

• Strep. viridens- endocarditis, urinary infection

• Strep. fecalis – urinary infection, pyogenic

infection

• Strep. pneumoniae – pneumonia, meningitis



Fungi

•

Fungi of relevance to surgeons: – cause nosocomial infections in surgical patients as

part of polymicrobial infections or fungemia (e.g.,C. albicans )

–

causes of aggressive soft tissue infections (e.g., Mucor , Rhizopus, and Absidia spp.)

– opportunistic pathogens that cause infection inthe immunocompromised host (e.g., Aspergillusfumigatus, niger , terreus, and other spp.,Blastomyces dermatitidis, Coccidioides immitis,and Cryptococcus neoformans)



Prevention and Treatment of

Surgical Infections



• Prophylaxis — are maneuvers todiminish the presence of exogenous(surgeon and operating room

environment) and endogenous(patient)



• Empiric therapy comprises the useof an antimicrobial agent or

agents when the risk of a surgicalinfection is high.



Infections of Significance in

Surgical Patients



Surgical Site Infections

• infections of thetissues, organs, or spaces exposed bysurgeons during

performance of aninvasiveprocedure.

• classified into: – Incisional

• superficial

• deep

– organ/spaceinfections



SURGICAL SITE INFECTION

DEFINITION

• Deep Incisional /Organ / Space Infection• Any infection occuring within postoperative 30 days or

within postoperative one year if any implant is left•

described as;• Presence of any purulant discharge (through drains)• Any positive culture findings from intraabdominalsamples• Spontaneous wound dehiscence

• Presence of abscess • Infection diagnosis determined by the surgeon



Factors Related to Developmentof SSIs

1. the degree of microbialcontamination of the wound duringsurgery

2. the duration of the procedure

3. host factors

• diabetes, malnutrition, obesity, immune

suppression, and a number of other underlying disease states.



Diagnosis

• • Redness

• • Swelling

• •

Hyperthermia • • Fluctuation

• • Purulent or turbid aspirate



Classification of Surgical Wounds

• Clean wounds (class I)

• Clean/contaminated wounds (class II)

• Contaminated wounds (class III)

• Dirty wounds (class IV)



a. CLEAN WOUND (I):

Elective cases, primarily closed andundrained

Nontraumatic, uninfected, noinflammation

Respiratory, alimentary,

genitourinary or oropharyngealtracts not entered

Hernia repair, breast biopsy



B. CLEAN – CONTAMINATED WOUND:

Alimentary, respiratory, genito-urinary

tract entered under controlled

conditions and w/o unusual

contamination Minor break in technique

Mechanical drainage

Appendectomy, biliary tract



C. CONTAMINATED WOUND

Open, fresh traumatic wound

Gross spillage from gastrointestinal tract

Entrance of genitourinary or biliary tracts

in presence of infected urine and bile

Major break in technique

Penetrating abdominal trauma, large

tissue injury, enterotomy during bowelobstruction



D. DIRTY AND INFECTED WOUND

Traumatic wound with retaineddevitalized tissue, foreign bodies,fecal contamination or delayed

treatment Perforated viscus encountered

Acute bacterial inflammation with pus

encountered during operation



Surgical management of the wound

In healthy individuals, class I and II woundsmay be closed primarily, while skin closure ofclass III and IV wounds is associated with high

rates of incisional SSIs (25 to 50%).

Class III and IV wounds should be packed

open and allowed to heal by secondary

intention, although selective use of delayedprimary closure has been associated with a

reduction in incisional SSI rates.



Intra-Abdominal Infections



• Peritonitis or intra-abdominal

infection — microbial contamination ofthe peritoneal cavity

• Primary microbial peritonitis — when

microbes invade the normally sterileconfines of the peritoneal cavity viahematogenous dissemination from adistant source of infection or directinoculation



Secondary microbial peritonitis occurssubsequent to contamination of the

peritoneal cavity due to perforation or severe inflammation and infection ofan intra-abdominal organ.



• postoperative peritonitis, or tertiary(persistent) peritonitis – seen in patientsin whom standard therapy fails, thus

an intra-abdominal abscess develop,and leakage from a GI anastomosisoccurs



Infections of the Skin and Soft

Tissue

E i l



Erysipelas

• Superficial spreading

cellulitis & lymphangitis• Area of redness,

sharply definedirregular border

• Follows minor skininjuries

• Streptococcuspyogenes

• Common site: aroundnose extending to bothcheeks

• Penicillin, Erythromycin



Cellulitis

• Inflammation of skin& subcutaneoustissue

• Non-suppurative

•

Strep. Pyogenes• Common sites- limbs

• Affected area is red,hot & indurated

• Treatment : – Rest, elevation of affected

limb..

Penicillin,Erythromycin,



This patientpresented with

spreadingcellulites and

pain on motionof his right hip 2

weeks after totalcolectomy.

Cellulitis on right

anterior thigh isoutlined

NECROTIZING FASCIITIS



NECROTIZING FASCIITIS

• Necrosis of superficial

fascia, overlying skin

• Polymicrobial

strep, staph, enterococci,

bacteroides, enterobacteriaceae

• Sites- abd.wall ( Meleny’s ) ,

perineum (Fournier’s) ,

limbs,

• Usually follows abdominal surgery or trauma



• More in diabetic patient

• Starts as cellulitis, edema, systemic toxicity

• Appears less extensive than actual

necrosis• Treatment:

Debridement , repeated dressings, skingrafting

Broad spectrum antibiotics ampicillin, clindamycin, aminoglycosides

severe late necrotizing fasciitis and



severe late necrotizing fasciitis andmyositis due to beta-hemolytic

streptococcal infection



STAPHYLCOCCAL INFECTIONS•

Abscess- : Localized accumulation ofpurulent

material situated in the dermis or subcutaneous

tissue. Treatment- drainage, antibiotics

• Furuncle- infection of hair follicle / sweatglands

• Carbuncle- extension of furuncle into subcutaneous tissue

common in diabetics

common sites- back, back of neck

Treatment: drainage, antibiotics,

control diabetes



P t ti N i l



Postoperative Nosocomial

Infection•

SSI

• UTI -dx: > 104 CFU/ml of microbes by

culture in symptomatic patients or >105 CFU/ml in asymptomatic pxs

• Pneumonia -prolonged mechanicalventilation

• Intravascular catheter infections



Sepsis



• Sepsis- is a potentially life threateningcomplications of an infection, occurswhen chemicals released into the

bloodstream to fight the infectiontrigger inflammation throughout thebody.



Nutrition in the Surgical

Patient

Estimation of Energy



Estimation of Energy

Requirements

• Basal energy expenditure (BEE) mayalso be estimated using the Harris-Benedict equations:

• where W = weight in kilograms; H = height incentimeters; and A = age in years.



M k f M l t iti



Markers of Malnutrition

Unintentional weight loss= ↑ complications

– % weight loss= (usual wt – present wt) x 100

usual wt

<10% - mild malnutrition, over 1 month

10-20%- moderate malnutrition, over 1

month

>20% - severe, in 6 months• >30% - pre-morbid

• >50% - pre-mortality

C l l ti f C l i d



Calculation of Caloric Needs

Condition Kcal/kg/day Protein/kg/day NPC : N ratio

Normal tomoderate

malnutrition

25 - 30 1 150 : 1

Moderatestress

25 - 30 1.5 120 : 1

Hypermetabolic, stressed

30 - 35 1.5 – 2.0 90-120 : 1

Burns 35 - 40 2.0 – 2.5 90-120 : 1



Indications

Patients who are nutritionally depleted

Patients who are unable to take nutrients byGI Tract

Those who should not take nutrients by the GItract because of an inherent risk or complicate

management of their current surgical disease



Indications for Nutritional Support

Short gut syndrome – <0.5 m jejunum/ileum

if with colon

– <1.0 m of small bowel

if without colon

Severely

malnourished

* All other indications are less clear




Patient not expected to feed in 7 days

– Prolonged ileus or intestinalobstruction




Patient not expected to feed in 7 days – Entero-cutaneous fistulas




ESOPHAGECTOMY COLON REPLACEMENT

CAUSTIC INGESTION, ESOPHAGEAL STRICTURE




Duodenal Leak Gastro-duodeno-pancreatectomy

Ro te of Administration:



Route of Administration:

1. ENTERAL ROUTE

2. PARENTERAL ROUTE (TPN)

3. COMBINATION

ENTERAL



ENTERAL

Advantages:1. more physiological (liver not

bypassed)

2. lesser cardiac work

3. safer and more efficient

4. better tolerated by the patient

5. more economical



ENTERAL NUTRITION

• Enteral access

– NGT

– Gastrostomy

–

Jejunostomy – PEG (percutaneous

endoscopicgastrostomy)

–

Trans-gastric jejunostomy

ENTERAL



ENTERALRoute:

1. Naso-enteric tube feeding (blended food – Casseinates and whole protein formulas)

Naso-esophageal or NGT / NJT.

2. Gastrostomy tube (blended food)

Stamm (sero-lined) – temporary

Glassman (mucous-lined) – permanent

Percutaneous endoscopic gastrostomy

3. Jejunostomy tube (elemental diet) Roue-en-y - permanent

Witzel - permanent

Endoscopic

ENTERAL



ENTERAL

Hyperosmolar solution are better tolerated by the stomach:

– Gastric feeding – increase osmolality firstthen the volume

–

Small bowel – volume first is increase thenosmolality



Rationale for Enteral Nutrition

• Enteral nutrition generally is preferredover parenteral nutrition, based on thelower cost of enteral feeding and the

associated risks of the intravenousroute, including vascular access

complications.



• The presence of bowel sounds and the

passage of flatus or stool are notabsolute prerequisites for initiation ofenteral nutrition.

•

Gastric residuals of 200 mL or more in a4- to 6-hour period or abdominaldistention requires cessation of feedingand adjustment of the infusion rate.

Decision Making



GIT functional?

YES NO

ENTERAL ROUTE PARENTERAL ROUTE

Short term Long term Short term Long term

NGT Gastrostomy,

Jejunostomy

Peripheral PN Central PN

Decision Making

Enteral versus Parenteral



Enteral versus Parenteral

• Blunt and penetratingabdominal trauma

early enteral feeding (Moore

1986 & 1989, Kudsk 1992, 1996) severity = complications if

feed enterally

• Severe head injury

– No benefit (Rapp 1983, Hadley 1986,Young 1987, Borzotta 1984)

– Beneficial (Grahm 1989)

Enteral vs Parenteral



Enteral vs. Parenteral

• General Surgery – Laparotomy

• Enteral better than parenteral) – Ulcerative Colitis and CD after resection

• Enteral better than parenteral –

Liver transplantation• Enteral = Parenteral (Wicks 1994 Level I evidence)

– Acute pancreatitis• Gastric and duodenal feeding- ↑

complication (Ragins 1973)

• TPN, jejunal feeding (Stabile 1984, Bodoky 1991)

• Jejunal feeding = TPN (McClave 1997 Level I evidence)

• Jejunal feeding better than TPN (Windsor 1998 Level Ievidence)

ENTERAL NUTRITION



ENTERAL NUTRITION

Nutritional Support Needed?

Parenteral Nutrition



As Supportive Therapy:

Nutritional support can be achieved but alterationin the disease process have not beenestablished.

New born GIT anomalies ( gastrochisis,omphalocele)

Alimentary tract obstruction (achalasia, stricture,carcinoma, pyloric obstruction)

Prolonged ileus

Prolonged respiratory support

Large wound losses


PARENTERAL NUTRITION




Proven efficacyRadiation & Chemoenteritis,

Hyperemesis gravidarum

Efficacy not yet establishedPre-op, cardiac cachexia, pancreatitis,

Ventilatory support, prolonged ileus

Under investigation

– Cancer, sepsis




Indications:Principal indication is found in seriously

ill patients suffering from Malnutrition,Sepsis, severe surgical or accidental

trauma when the use of theGastrointestinal tract for feeding is not possible.

Can be supplemental in patients withinadequate oral intake






• Primary Therapy – Proven efficacy

• GI fistulas

• Short bowel syndrome

• ATN, Hepaticinsufficiency

– Efficacy not established

• IBD, Anorexia nervosa




Parenteral NutritionContraindication of TPN:

1. Lack of specific goal for severe metabolicmanagement (inevitable dying).

2. Cardiovascular instability / severe

metabolic derangement.3. Feasible GIT feeding

4. Patient with good nutritional status

5. Infants with less than 3cm of small bowel6. Irreversible decerebrate (dehumanized)





• Peripheral TPN

– 3% AA in 10% dextrose + 10% lipid

– Used when central line is

contraindicated – Short-term

• Central TPN

– 15-25% dextrose = standard formula – 47% dextrose = special formula

V A



Venous Access

S b l i A



Subclavian Access

Venous Access



Venous Access





Peripheral Central

Dextrose content < 5% > 10

Calorie delivery Less More

Volume delivery More Less

Calorie source* Mostly fats Mostly CHO

Calorie distribution CHO 30% CHON20% Fats 50%

CHO 55-60% CHON15-20% Fats 25%




As Primary Therapy:

– TPN influence the disease process:1. GIT fistula

2. Renal failure (ATN)

3. Short Bowel Syndrome

4. Acute Burn (severe trauma)

5. Hepatic failure

6. With normal bowel length but with

malabsorption syndrome due to SPRUE,enzymatic or pancreatic insufficiency,Ulcerative colitis, regional enteritis

7. Anorexia nervosa





Parenteral NutritionRoute of TPN:

Central

hyperalimentation

– Subclavian vein

–

Internal jugular vein – Femoral vein

Gauge 16, 8-12

inches radio-opaque

catheter end at SVCCheck position w/

x-ray





Complications of TPN:

I. Technical complications:

A. Early: - related to catheter insertion

1. Pneumothorax

2. Arterial laceration

3. Hemothorax

4. Mediastinal hematoma

5. Nerve injury to the brachial plexus

6. Hydrothorax

7. Air embolism

8. Catheter embolism





I. Technical complications:A. Late: Erosion of the catheter to the bronchus or right

atrium

Thrombosis: Upper arm swelling and pain at the base of the

neck

Streptokinase / heparin ---> coumadin

Septic thrombosis: Antibiotic therapy

Fogarty catheter embolectomy

Excision of the subclavian vein and superior

venacava





I. Technical complications:A. Late:

Erosion of the catheter to the bronchus or right atrium

Thrombosis:

Upper arm swelling and pain at the base of theneck

Streptokinase / heparin ---> coumadin

Septic thrombosis:

Antibiotic therapy Fogarty catheter embolectomy

Excision of the subclavian vein and superior

venacava





II. Metabolic complications:

A. Inadequate administration of certain

nutrient

1. Trace metal deficiency:a) Zinc deficiency:

perioral pustular rash

darkening of the skin creases

neuritis

b) Copper deficiency:

microcytic anemia






A. Inadequate cont’d

2. Essential Fatty Acid deficiency:

Dry flaky skin w/ small reddish papules andalopecia

B. Disorder of Glucose metabolism:

1. Hypoglycemia – unexpected slowing of theglucose infusion / excessive insulinadministration





II. Metabolic complications:B. Disorder of Glucose metabolism:

2. Hyperglycemia – most dangerous metabolismcomplication in TPN

Due to rapid infusion (60 ml/hr the increaseof 20ml/hr every 24-48 hrs)

DM ( Hyperosmolar nonketotic coma) dueto osmotic diuresis ---> dehydration, fever,obtundation and coma ---> death.

Tx: insulin 200 units/day and administrationof large dextrose free hypo=osmolar solution (0.45% NSS w/ K+).






C. Liver function derangement:

Abnormalities in SGOT / SGPT / Alk.

PO4 Fatty infiltrate of liver ----> fat

emulsion





III. Septic complications:A. Catheter infection: most lethal complication of TPN Bacterial / fungal (candida) Site of entry of the organism ---> site of

catheter Symptom: - sudden spike of fever Management:

− Change TPN bottle, tubes and filter –

culture / investigate for presence ofpneumonia, UTI, wound infection, etc.− If fever persist after 8 hrs. ---> removed

catheter and culture the tip of the tube.




Thank You!

Surgical infection and Nutrition

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