THE PANCREAS AND

ANESTHESIA
Martha Richter, MSN, CRNA

THE PANCREAS

THE PANCREAS
EXOCRINE FUNCTIONS
Pancreatic digestive enzymes secreted
by pancreatic acini
NaBicarb secreted by ducts & ductules
Combined, they flow thru pancreatic
ductjoin hepatic ductenter
duodenum thru papilla of vater,
surrounded by sphincter of Oddi

THE PANCREAS
ENDOCRINE FUNCTIONS
Involved with metabolism
carbohydrates and blood sugar
regulation
Insulin secreted directly into blood
Islets of Langerhans patches
throughout gland
Composed of

Alpha cells =25%Glucagon

Beta cells=60%insulin and amylin
Delta cells=10%somatostatin
PP cellspancreatic polypeptides

THE PANCREAS
Conditions for this lecture
Pancreatitis-acute & chronic
Pancreatic cyst/psuedocyst
Pancreatic CA
Diabetes
Insulinoma

ACUTE PANCREATITIS
The acute inflammatory
process-autodigestion
60-80% caused by ETOH and
cholelithiasis
Also seen in patients with
AIDS
Hyperparathyroidism (inc Ca++)
Blunt abdominal trauma
Postoperative abdominal surgery
Thorac surgery postop, CABG
1-2% post ERCP

ACUTE PANCREATITIS
S&S
Severe epigastric pain radiating to back
N&V
Abdominal distention
Dyspnea b/o pleural effusions, ascites
Fever
Shock
Tetany b/o hypocalcemia
Obtundedpsychoses
Withdrawal in alcoholics

ACUTE PANCREATITIS
Remember the comorbidities
ETOH abuse
Malnourishment
ETOH withdrawal

ACUTE PANCREATITIS
Diagnosis
Elevated serum amylase
CT scan
ERCP to localize site of trauma,
existence of obstruction
Differential includes:

Perforated duodenal ulcer

Acute cholecystitis
Mesenteric ischemia
Bowel obstruction
Acute MI
pneumonia

ACUTE PANCREATITIS
Complications=25%
Shock early=major cause of death b/o
sequestration fld in peripancreat sp,
hemorrhage, dec SVR
ARDS=20%arterial hypoxemia
Renal failure=25%poor prognosis
GI hemorrhage
DIC
Pseudocyst formation=10-15%(b/o
hemorrhage & resolution)
Pancreatic infection=50% mortality
when strictures develop

ACUTE PANCREATITIS
RX=supportive
Aggressive IV fld admin
If hemorrhagiccolloids, blood
products
NPO
N/G for persist vomiting/ileus
Opioids
Prophylactic antibiotics if
necrotizing
Endoscopic removal of stones
Parenteral nutrition

ACUTE PANCREATITIS
RX
Surgery may be required for
complications
Surgical debride for necrotic pancreas
Hemorrhagic panc. Unresponsive to
blood prod resusc and correction
coagulopathies
Drainage pseudocysts

ACUTE PANCREATITIS
ERCP
Endoscopic Retrograde
Cholangiopancreatography
Allows dx re: liver, GB, pancreas,
bile ductspresence of jaundice,
abdominal pain, unexplained wt loss

ERCP
MAC
Throat sprayedloss airway
protection
LLD position
Sedation
When ducts reached, patient
positioned supine
Dye injected into ductsvisualized
with xrays.
If obstr=stones, removed. If obstr =
tumor, bx may be taken

ERCP
Pt experiences pain when:
duodenum insufflated with air and
dye injected
If stone is removedovernight
observation in hospital
Need to know: Iodine allergy?

ERCP
Complications
Pancreatitis
Infection
Bleeding
Duodenal perforation (uncommon)

ACUTE PANCREATITIS AND SURGERY

POSTOP COURSE-ICU probable
b/o activation of inflammatory
mediators, may see
Sepsis
Multi organ dysfunction
Fld resuscitation

PPV
pressors

CHRONIC PANCREATITIS
Chronic inflammationirreversible
damage of pancreas
Pain may be attributed to other
causes
May have recurrent attacks
Symptoms may be progressive

CHRONIC PANCREATITIS
35-45 yr males
80-90% ETOH associated
Concurrent high protein diets

CHRONIC PANCREATITIS
Idiopathic
Second most common
May be seen with cystic fibrosis,
hyperparathyroidism, hereditary
(autosomal dominant)
CHRONIC OBSTRUCTION PANCRATIC
DUCT

CHRONIC PANCREATITIS
PRESENTATION
Postprandial epigastric pain radiating
to back
10-30% painless
Steatorrhea when 90% pancreas
destroyed
Eventually develop DM
Calcifications develop in ETOH induced

CHRONIC PANCREATITIS
DIAGNOSIS
h/o ETOH, pancreatic calcifications
Thin & emaciated
Malabsorp syndromeproteins & Fats
not digest when enzymes reaching
duodenum=10-20%
Normal serum amylase
Abd Xray=calcifications
U/S=identifies fluid filled pseudocysts,
enlarged pancreas
CT=dilated pancreatic ducts
ERCP=detects early changes in duct

CHRONIC PANCREATITIS

TREATMENT
Pain treatment
Malabsorption management
DM management(30-40% develop)
Drain pancreas:
pancreatojejunostomy, stents, stone
extraction
Enzyme supplements
Pseudocyst resect
(open/percutaneous)
Paracentesis/thoracentesis

CHRONIC PANCREATITIS AND PAIN

Managed with
Opioids
Celiac plexus block

CHRONIC PANCREATITIS & ANESTHESIA

Evaluation:
Status of ETOH
CV complications re: ETOH
Status of DM
Method of pain management (is it
working?)
Consider state of malnutrition and
effect of anesthetic drugs, distribution
Keep the patient warm
Be alert for withdrawal under
anesthesia

PANCREATIC CANCER

5th leading cause Cancer death in US

Females
60 years+
Usually not detected early
Responds poorly to RX
Spreads quickly

PANCREATIC CANCER
Risk factors
Cigarette smoking accelerates tumor
growth
Family history
Hereditary syndromes = younger
patients

PANCREATIC CANCER
S&S
Jaundice b/o bile duct obstruction
N/V
Loss of appetite
Wt loss (unexplained)
Mid abd pain radiating to back
(indicates splanchnic & retroperitoneal
invasion)
Dark urine
Light stools
DM development=rare

PANCREATIC CANCER
STAGING OF MALIGNANCY
I very small tumor, limited to
pancreas
II larger tumors limited to pancreas
III lymph node spread
IV metastatic to colon, spleen,
stomach and distant organs
(liver,
lungs)

PANCREATIC CANCER
95% begin in ducts
Usually adenocarcinoma
Occurrence in tail = rare

PANCREATIC CANCER
RX
Biopsy to confirm
(endoscopic/radiologic)
Pain management
If no spread, surgery = best option.
Surgical mortality 1-15%
Preop chemo and radiation to shrink
tumor

PANCREATIC CANCER
If metastatic, goal = palliation
ERCP to open obstructed duct
Pain management may include
narcotics, celiac plexus block
Chemo
Radiation
Unresected survival = 5 months

PANCREATIC CANCER
Surgery
Total pancreatectomy
Pancreaticoduodenectomy (Whipple)

PANCREATIC CANCER
Total Pancreatectomy
Surgically easier to perform
Produces DM and malabsorption states
10% survival = 5 years

PANCREATIC CANCER
WHIPPLE
Major morbidity b/o:
Cardiopulmonary disease
Pancreatic/biliary fistula
Hemorrhage
infection

PANCREATIC CANCER
WHIPPLE
Big procedureshould be done in
big hospital setting

Bowel prep = require rehydration

Type and crossmatch
Usual systems evaluation
If obstructedprepare for RSI (pre
treat regimen)

PANCREATIC CANCER
WHIPPLE
Anesthesia plan
GA
GA/Epi (lumbar/thoracic)

Monitors incl CVP, art line

Large bore IVs-there will be large fld
shifts, blood loss
RSI in the face of obstruction
Warm the patient
Warm the fluids

PANCREATIC CANCER
WHIPPLE
Have the blood in the room and
checkedpossibility of portal v or
vena cava injury
May require mesenteric vessel and
portal v resection
Remember the comorbidities
Prepare for postop PPV if massive
blood loss/replacement

PANCREATIC CANCER
WHIPPLE
In the face of the best planned
anesthetic, Plan B must include
possibility of open and close

DIABETES
Chronic disease
Relative lack/lack of insulin
Inappropriate hyperglycemia

DIABETES
TYPE I or IDDM
Juvenile onset
Brittle (more prone to ketosis)
Have very low insulin levels
Require Insulin

DIABETES
TYPE II OR NIDDM
Makes up 90% of all diabetics
gradual onset
usually overweight
not prone to ketosis
have insulin resistance
at inc risk for hyperglycemic
hyperosmolar nonketotic coma
(HHNK)
RX=diet, oral hypoglycemics, occas.
insulin

DIABETES
What else can cause it?
Diseases that alter hormone levels
Acromegaly
Glucogonoma
Cushing's
Pheochromocytoma
ALSO:
Pancreatic
damage/destruction(surgery)
Cystic fibrosis
hemochromatosis

DIABETES
Manifestations
Hyperglycemia
Glycosuria
Degeneration of small blood vessels

DIABETES
Long term complications =
morbidity, premature mortality
Late complications = HTN, CAD,
PVD, cereb vasc dis, retinopathy,
nephropathy, peripheral and
autonomic neuropathies
Life threatening complications =
hypoglycemia, ketoacidosis,
HHNK coma

DIABETES
KETOACIDOSIS
Caused by stress
Infections, surgery, trauma

Poor pt compliance may be

implicated
Can be soon post-MI

DIABETES and ketoacidosis

Presentation
N/V
Sensorium changes
Dyspnea (comp for metabol. Acidosis)
Abdominal pain
Hyperglycemia (300-500mg/dL)
Hyperosmolarity
Intracellular dehydration
Osmotic diuresisprofound
hypovolemia
Hyperkalemia
hyponatremia

DIABETES AND KETOACIDOSIS

RX
Correction dehydration, hyperglycemia,
K+ deficiency
Isotonic fluids
Insulin infusion
K+ replacement

DIABETES AND HYPOGLYCEMIA

DEF:excessive insulin relative to
carbohydrate intake= bld
glucose<50mg/dL
Brain=most susceptible
Uncorrected=confusion, fainting
progressing to seizures, coma
Systemic effects b/o catecholamine
discharge: tachycardia, HTN,
diaphoresis (may be marked under
GA)
True level varies patient to patient

DIABETES AND HHNK COMA

Plasma hyperosmolarity >330mOm/L
Hyperglycemia >600mg/dL
Marked osmot diuresisloss K, Na, vol

Profound dehydration
Leads to lactic acidosis, renal failure,
predisposition to venous thrombosis

Absence ketoacidosis (pt has

enough insulin to avoid ketosis)

DIABETES AND HHNK COMA

S&S
Altered mental statecoma

RX
Fluid resuscitation
Small doses IV Insulin
K+ supplement
When glu reaches 300mg/dL, Rx slows
to prevent cerebral edema
Triggered by: infection, trauma,
dehydration; more common in elderly
May occur in diabetics/nondiabetics

DIABETES AND ANESTHESIA

Preop assessment
Correct glucose abnormalities
Check for electrolye abn
Correct ketoacidosis

DIABETES AND ANESTHESIA

Periop morbidity re: end organ
damage
Eval CV, cereb, renal systems
Diabetic neuropathy may manifest:
Painless MI (silent)
Orthostatic hypotension
Resting tachycardia
Lack HR variability
Gastroparesis
Impotence
Dec sensation peripheral

DIABETES AND ANESTHESIA

When diabetics have neuropathy
affecting autonomic function, they
are at high risk of aspiration, intraop
cardiac instability, sudden cardiac
death.

DIABETES AND ANESTHESIA

Aspiration prophylaxis
Preop cocktail
Rapid sequence induction

Invasive monitoring
Strict aseptic technique when placing
b/o compromised immune system

DIABETES AND ANESTHESIA

INTRAOP GOALS
Prevent hypoglycemia
Prevent hyperglycemia and
ketoacidosis
Maintain bld glu 120-180mg/dL
Monitor blood glucose at intervals
approp to case

DIABETES AND ANESTHESIA

Be familiar with oral hypoglycemia
agents, onset and duration. This
influences when a patient may
become hypoglycemia while under
your care.

DIABETES AND ANESTHESIA

Drug-1st gen

Rel potency

Dur-h

Tolbutamine

6-10

Acetohexamide

2.5

12-18

tolazamide

16-24

Chlorpropamide

24-72

Glyburide

150

18-24

glipizide

100

16-24

2nd gen

DIABETES, INSULIN AND ANESTHESIA

3 possible approaches for insulin
management during anesthesia
Pt takes -1/2 total a.m. dose in form
of intermediate acting insulin.
Consider D5 soln to prevent
hypoglycemia. If hypoglycemia
develops (50-100mg/dL), give 10gms
D50will raise bld Glu 30-40mg/dL

DIABETES, INSULIN AND ANESTHESIA

A second approach:
IV regular insulin may be given
according to a sliding scale.
1 Unit regular insulin will decrease bld
glucose 25-30mg/dL in an adult

DIABETES, INSULIN AND ANESTHESIA

A 3rd approach
Run an IV Insulin infusion at 1Unit/hr

No matter what approach is chosen,

remember to monitor the blood glucose
at regular intervals (preop, intraop,
postop)

DIABETES, INSULIN AND ANESTHESIA

INSULINS ONSET

PEAK

DURATION

FAST ACTING
REGULAR

30-60 MIN

2-4 HOURS

5-7 HRS

SEMI-LENTE

30-60 MIN

4-6 HOURS

12-16 HRS

ISOPHANE(nph

1-2 HOURS

10-20 HOURS

18-24 HRS

LENTE

1-3 HOURS

14-18 HOURS

20-24 HRS

PROTAMINE
ZINC

4-6 HOURS

16-22 HOURS

25-36 HRS

ULTRALENTE

4-6 HOURS

24 HOURS

25-36 HRS

INTERMEDIATE

LONGACTING

DIABETES AND ANESTHESIA

AVOID HYPOGLYCEMIA
Improved glycemic
managementimproved
perioperative M&M
HbA1c <7.5%=adequate control
Schedule patients early to limit NPO
Remember to d/c metformin 2 days
preop (rare possibility of producing
lactic acidosis)

DIABETES AND ANESTHESIA

What about insulin pumps?
Different philosophies:
May continue infusion if not in
operative field
Some will always discontinue; restart in
PACU

If continue or d/cremember to
monitor the bld glucose levels at
frequent intervals

DIABETES AND ANESTHESIA

What about emergencies?
Common for diabetics to require
appendectomies, I&Ds, lower extremity
amputations (infect/vasc insuff)

Evaluate mental status, labs

If presenting with ketoacidosis, Rx
1st with IV Insulin, K+ replace, fluid
vol replacement.
CVP may be helpful

INSULINOMA
Beta Islet cell tumorsprofound
hypoglycemia b/o excess release
Insulin
CNS=dizziness to coma

INSULINOMA
S&S
Hypoglycemia (tachycardia, HTN,
diaphoresis
May be masked by GA
RX: surgical excision of tumor

INSULINOMA
Want to start an Insulin infusion
prior to induction
Some recommend bld glu measures
q 15 min
Glu fluctuates widely with:
Tumor manipulation (hypoglycemia)\
Tumor excision (hyperglycemia)

The POST-PANCREATIC TRANSPLANT PATIENT

The actual considerations of the
transplant surgery will be covered in
the transplant lectures
What about taking care of these
patients after the Tx?
The transplant effectively restores
glucose metabolism
These patients will not require insulin
coverage
Always assume IHD

The PANCREAS AND ANESTHESIA

CONSIDERATIONS
Just as with most other physiologic
issues, this patient population will
have comorbidities. It is important
to appreciate the influences and
interactions that exist so that we
may approach the plan of care in a
careful, logical, thoughtful way.