Abdominal compartment syndrome

refers to organ dysfunction caused by

intraabdominal hypertension (IAH).

It may be under-recognized because:

-it primarily affects patients who
are already quite ill
-organ dysfunction may be
incorrectly ascribed to progression of
the primary illness.
Since treatment can improve organ
dysfunction, it is important that
the diagnosis be considered in the
appropriate clinical situation
without any delay
Intraabdominal hypertension
(IAH) and abdominal
compartment syndrome
(ACS) are distinct clinical
entities and should not be
used interchangeably.
Intraabdominal pressure (IAP) :
It is the steady state pressure concealed
within the abdominal cavity. For most
critically ill patients, an IAP of 5 to 7
mmHg is considered normal.

Patients with increased abdominal girth

that developed slowly e.g. the mobidly
obese and pregnant individuals may
have chronically higher baseline IAP (as
high as 10 to 15 mmHg) without adverse
sequelae
Abdominal perfusion pressure
(APP):
It is calculated as the mean
arterial pressure (MAP) minus
the IAP
APP = MAP - IAP.

Elevated IAP reduces blood

flow to the abdominal
viscera
Abdominal perfusion pressure
(APP) was found to be better
than other resuscitation
endpoints e.g. hourly urinary
output for predicting the
outcomes.

A target APP of at least 60 mmHg

is correlated with improved
survival from IAH and ACS.
Intraabdominal hypertension
(IAH)
It is defined as a sustained
IAP
of ≥12 mmHg.
Intraabdominal hypertension
(IAH) can be further graded as
follows:
-Grade I = IAP 12 to 15
mmHg
-Grade II = IAP 16 to 20
mmHg
-Grade III = IAP 21 to 25
mmHg
- Grade IV = IAP >25
mmHg.
Hyperacute IAH :
-Elevation of the IAP lasting only
seconds.
-It is due to laughing, coughing,
straining, sneezing, defecation, or
physical activity. IAH with ACS due to
gastric over-distention following
endoscopy has been described.

Acute IAH:
-Elevation of the IAP that develops over
hours.
-It is usually the result of trauma or
intraabdominal hemorrhage and can lead
to the rapid development of ACS.
Subacute IAH :
-Elevation of the IAP that develops
over days.
-It is most common in medical
patients and can also lead to ACS.

Chronic IAH:
-Elevation of IAP that develops over
months (pregnancy) or years
(morbid obesity).
-It does not cause ACS, but does
place the individual at higher risk for
ACS if they develop superimposed
acute or subacute IAH.
Abdominal compartment syndrome
(ACS):
- It is defined as a sustained IAP
>20 mmHg (with or without APP
<60 mmHg) that is associated with
new organ dysfunction.

For clinical purposes, ACS is better

defined as IAH-induced new organ
dysfunction without a strict IAP
threshold, because no IAP can
predictably diagnose ACS in all
patients.
 Patients with an IAP < 10
mmHg generally do not have
ACS, while patients with an IAP
> 25 mmHg usually have
ACS.

Patients with an IAP 10-25

mmHg may or may not have
ACS, depending upon individual
variables such as blood pressure
and abdominal wall
compliance.
Higher systemic blood
pressure may maintain
abdominal organ perfusion
when IAP is increased, since
the abdominal perfusion
pressure (APP) is the
difference between the mean
arterial pressure and the
IAP.
Abdominal wall compliance initially
minimizes the extent to which an
increasing abdominal girth can elevate
IAP .

-When a critical abdominal girth is

reached, abdominal wall compliance
decreases abruptly. Further increases
in abdominal girth beyond this critical
level result in a rapid rise of IAP and
ACS if untreated.

-Increased abdominal wall

compliance due to chronic increased
abdominal girth (e.g. pregnancy,
cirrhosis with ascites, morbid obesity)
may protect against ACS .
The incidence of IAH is less
well characterized.
-The incidence of ACS in
trauma patients varies
considerably.
-It ranges from 1 to 14
percent in different studies.
ACS was considered present if there was:

- persistent IAH
- progressive organ dysfunction
despite resuscitation and
- improvement following
decompression
ACS can be classified as:
- Primary ACS is due to injury or disease in
the abdominopelvic region (e.g. abdominal
trauma, hemoperitoneum, pancreatitis);
intervention (surgical or radiologic) of the
primary condition is often needed.

- Secondary ACS refers to conditions that

do not originate in the abdomen or pelvis
(e.g. fluid resuscitation, sepsis, burns).

- Recurrent ACS defines a condition in

which ACS develops again following
previous surgical or medical treatment of
primary or secondary ACS
ACS generally occurs in patients who are critically ill due to any of a wide
variety of medical and surgical conditions. Some of these include:
-Trauma : Injured patients in shock who require aggressive fluid
resuscitation are at risk for ACS.

- Burns: Patients with severe burns (>30 percent total body surface
area) with or without concomitant trauma are also at risk for ACS.
Importantly, ACS must be distinguished from other intraabdominal
problems that occur in these critically ill patients (eg, necrotizing
enterocolitis, ischemic bowel).

- Liver transplantation: IAH (IAP >25 mmHg) was found following liver
transplantation in 32% patients.

- Abdominal conditions : Massive ascites, bowel

distension, abdominal surgery, or intraperitoneal bleeding can
increase intraabdominal pressure.

- Retroperitoneal conditions: Retroperitoneal pathologies, such as

ruptured abdominal aortic aneurysm, pelvic fracture with
bleeding, and pancreatitis, can lead to ACS.

- Medical illness: Conditions that require extensive fluid

resuscitation (e.g. sepsis) and are associated with third spacing of
fluids and tissue edema can increase IAP.

- Post-surgical patients: Patients undergoing operations in which

they are given large volume resuscitation, particularly with crystalloid
in the face of hemorrhagic or septic shock, are at risk for ACS.
IAH can impaire the function of
nearly every organ system,
thereby causing ACS .
It is desirable to recognize IAH early, so it
can be treated before progressing to
ACS.

Symptoms:
-Most patients who develop ACS are
critically ill and unable to communicate.

-The rare patient who is able to convey

symptoms may complain of malaise,
weakness, lightheadedness, dyspnea,
abdominal bloating, or abdominal pain.
Physical signs:
-Nearly all patients with ACS have
a tensely distended abdomen.
Despite this, physical examination
of the abdomen is a poor
predictor of ACS.

-Progressive oliguria and

increased ventilatory
requirements are also common in
patients with ACS.
- Other findings may include
hypotension, tachycardia, an
elevated jugular venous pressure,
jugular venous distension,
peripheral edema, abdominal
tenderness, or acute pulmonary
decompensation.

- There may also be evidence of

hypoperfusion, including cool skin,
obtundation, restlessness, or
lactic acidosis
Imaging findings:
- Imaging is not helpful in the diagnosis of
ACS.

-CXR may show decreased lung volumes,

atelectasis, or elevated hemidiaphragms.

-Computed tomography (CT) may

demonstrate tense infiltration of the
retroperitoneum that is out of proportion
to peritoneal disease, extrinsic
compression of the inferior vena cava,
massive abdominal distention, direct
renal compression or displacement,
bowel wall thickening, or bilateral
inguinal herniation
Definitive diagnosis of
ACS requires
measurement of the
IAP.

This is particularly true for

patients who have trauma,
liver transplantation, bowel
obstruction, pancreatitis,
or peritonitis because
these conditions are known
to be associated with ACS.
Measurement of intraabdominal
pressure:
- IAP can be measured indirectly
using intragastric, intracolonic,
intravesical (bladder), or inferior
vena cava catheters.

Measurement of bladder (ie,

intravesical) pressure is the
standard method to screen for IAH
and ACS. It is simple, minimally
invasive, and accurate.
Postoperative (abdom. Surgery) pts
Pts with abdominal trauma
Ventilated pts with other Organ
Failure
Pts with signs of ACS:
 Oliguria, hypoxia, hypotension,
acidosis, mesenteric ischemia, ileus,
elevated ICP.
Pts with high cumulative fluid balance
Pts with abdominal packing
Management of IAH and ACS
consists of supportive care
and, when needed, abdominal
decompression.

Some exceptions include

escharotomy release to relieve
mechanical limitations due to
burn eschars and percutaneous
catheter decompression to relieve
tense ascites.
Supportive care:
- Goals:
-Reduction of intraabdominal
volume.

- Measures to improve abdominal

wall compliance .
Nasogastric and rectal drainage
are a simple means for
reducing IAP in patients with
bowel distension.

Hemoperitoneum, ascites, intra

abdominal abscess and
retroperitoneal hematoma
occupy space and can elevate
IAP. In some cases, these
collections can be evacuated
using percutaneous techniques.
Patient should be placed in a supine
position.

Abdominal wall compliance can be

improved with adequate pain
control and sedation.
Ventilatory support:
- High peak and mean airway
pressures can be problematic.
Tidal volume reduction, a
pressure-limited mode, and/or
permissive hypercapnia may be
necessary.

Positive end-expiratory
pressure (PEEP) may
reduce ventilation- perfusion
mismatch and improve
hypoxemia.
Hemodynamic support:

-For patients with IAH, limiting

the amount of fluid
administration may decrease the
risk of developing ACS.

-Some clinicians prefer to use

colloids under this circumstance
instead of crystalloids.
There is no role for diuretic therapy
in the resuscitation of patients with
acute ACS.

The only appropriate management is

to open the abdomen.
SURGICAL DECOMPRESSION:
-There is general agreement that
surgical decompression is indicated
for ACS.

- Decompressing the abdomen

prior to the development of ACS is
becoming increasingly common
and may improve survival.
Various approaches include:
- Surgical decompression for
all patients whose IAP is
greater than 25 mmHg.

- Many clinicians suggest

surgical decompression at a
lower IAP (e.g. 15 to 25
mmHg.
Surgical decompression is considered
when the IAP is 20 mmHg or
greater, regardless of signs of ACS..

Most surgeons perform

decompression and then maintain
an open abdomen using temporary
abdominal wall closure.

Surgical decompression can be

performed in the operating room if
the patient is medically stable for
transfer or at the bedside in the
intensive care unit.
MORBIDITY AND MORTALITY:
- Failure to recognize IAH prior to the
development of ACS causes tissue
hypoperfusion, which may lead to
multisystem organ failure, and
potentially death.

- Although the development of IAH

alone is not a predictor of multiorgan
failure, mortality for patients who have
progressed to ACS range from 40 to
100%.
INTRODUCTION:
- Refers to a defect in the
abdominal wall that exposes the
abdominal viscera.

Damage control surgery associated

with trauma and ACS is the most
frequent reason for open
abdomen.
Etiology:
- The most common circumstances
that result in open abdomen include
the following:

1. Damage control surgery:

- It is an operative strategy that is used
to manage immediately life-
threatening conditions by delaying
definitive management of less severe
2. Abdominal compartment syndrome
(ACS):
-Increased volume in the abdomen is
typically the result of an increase
in interstitial fluid as is seen with
large volume resuscitation, but
space occupying fluid (blood or
ascites) in the peritoneum or
retroperitoneum can also
contribute.
3. Septic abdomen:
- Bowel perforation with severe
contamination of the peritoneal
cavity can result in recurrent intra-
abdominal sepsis.

- Under this circumstance, it may be

desirable to leave the abdominal
wall open and use negative-pressure
wound therapy to remove residual
or reaccumulated fluid or pus.
4. Refractory intracranial
hypertension :
- A more controversial indication
for open abdomen is refractory
intracranial hypertension
associated with traumatic brain
injury.
 Complications of open
abdomen:
Related to fluid efflux from the abdomen,
exposure of the bowel, and abdominal
muscle retraction.

- Fluid loss:
- A significant amount of fluid can be lost
through an open abdomen.

- Protein loss:
– The fluid that is secreted by the
peritoneum is rich in protein with about 2
grams of protein lost from the abdomen for
each liter of fluid removed.
- Fistula formation:
– With open abdomen, the bowel is
frequently manipulated and is at risk
for injury.

- Loss of domain:
- With open abdomen from a midline
abdominal incision, the musculature of
the abdominal wall retracts the fascia
laterally.

- The use of a negative pressure wound

system helps to counteract the lateral
forces on the abdominal wall and may
allow primary closure of the fascia and
skin .
Temporary closure techniques:
- In some patients, delayed primary
closure of the abdominal fascia is
possible once edema subsides.
However, if closure is premature,
ACS
can recur.
ABDOMINAL CLOSURE —
Each
time the patient is returned to
the operating room, the
abdomen is assessed for
potential closure.
 Fascial closure:

1. Primary fascial closure:

- Associated with the lowest rate
of complications following
management of the open
abdomen.

- Because of the high hernia rate,

biologic mesh reinforcement
during primary fascial closure is
frequently used.
2. Functional closure:

-Functional closure refers to the

bridging of a residual fascial
defect with a biologic mesh (in-
lay technique).

-Once the biologic mesh is

placed, the skin is closed over
surgical drains placed into
the subcutaneous space.
3. Planned ventral hernia:
- If primary fascial closure or
functional closure cannot
be achieved.
- Skin-only closure:
A skin-only closure
approximates the skin over the
fascial defect leaving a ventral
hernia.
 - Split-thickness skin
graft:
- If the skin cannot be
approximated, the viscera within
the wound are allowed to adhere
to each other and to the
abdominal wall. Once the
abdominal contents have
“solidified” and there is a
healthy bed of granulation tissue
overlying the bowel, a split-
thickness skin graft can be placed.
Increased IAP is called intraabdominal
hypertension (IAH). Abdominal
compartment syndrome (ACS) refers to
organ dysfunction caused by
intraabdominal hypertension.

ACS can impair the function of nearly

every organ system.

Diagnosis of ACS requires that IAP be

measured. Symptoms, physical signs,
and imaging findings are insufficient to
diagnose ACS.
Management initially consists of careful
observation and supportive care. In
some cases abdominal compartment
decompression is required.

We suggest that surgical

decompression is not delayed until the
development of ACS (Grade 2C).

Following surgical decompression, an

open abdomen is maintained using a
variety of temporary abdominal
closure techniques.
Following temporary abdominal
closure, the patient is monitored in
ICU.

- Abdominal dressings associated

with the closure (adhesive
dressings, gauze, negative pressure
systems) are changed, as needed,
and the abdominal contents
inspected every two to three days.
We suggest the use of a negative pressure
system (towel or sponge based) to control
and quantify fluid loss (Grade 2C).

Once the indication for the open abdomen

has resolved, the abdomen is
closed, preferably with a primary fascial
closure. If primary fascial closure cannot
be achieved, functional closure can be
performed.

If the gap between the fascia is deemed to

be too large for a functional
closure, primary skin closure can be
performed, or skin grafts placed once a
layer of granulation tissue has developed.
The message is:

- Be ACS-minded.
- Decompress early.
- Apply TAC techniques.
-Definitive abdominal
closure as early as
possible.
 CRITICAL CARE MANAGEMENT FOR RENAL FAILURE
Prepared by: Ryan Jay L. Yalung

What is Chronic Renal Failure?

 Chronic renal failure (CRF) is the end result of a gradual, progressive loss of
kidney function.
 Causes include chronic infections (glomerulonephritis, pyelonephritis),
vascular diseases (hypertension, nephrosclerosis), obstructive processes (renal
calculi), collagen diseases (systemic lupus), nephrotoxic agents (drugs, such
as aminoglycosides), and endocrine diseases (diabetes, hyperparathyroidism).
 This syndrome is generally progressive and produces major changes in all
body systems.
 The final stage of renal dysfunction, end-stage renal disease (ESRD), is
demonstrated by a glomerular filtration rate (GFR) of 15%–20% of normal or
less.
 Renal failure results when the kidneys cannot remove the body’s metabolic
wastes or perform their regulatory functions.
 The substances normally eliminated in the urine accumulate in the body fluids
as a result of impaired renal excretion, affecting endocrine and metabolic
functions as well as fluid, electrolyte, and acid-base disturbances.
 Renal failure is a systemic disease and is a final common pathway of many
different kidney and urinary tract diseases.
 Accumulation. As renal function declines, the end products of protein
metabolism (normally excreted in urine) accumulate in the blood.
 Adve rse effects. Uremia develops and adversely affects every system in the
body.
 Progression. The disease tends to progress more rapidly in patients who
excrete significant amounts of protein or have elevated blood pressure than
those without these conditions

Clinical Manifestations

 Peripheral neuropathy. Peripheral neuropathy, a disorder of the

peripheral nervous system, is present in some patients.
 Severe pain. Patients complain of severe pain and discomfort.
 Restless leg syndrome. Restless leg syndrome and burning feet can occur in
the early stage of uremic peripheral neuropathy.

Complications

 Hype rkalemia. Hyperkalemia due to decreased excretion, metabolic acidosis,

catabolism, and excessive intake (diet, medications, fluids).
 Pericarditis. Pericarditis due to retention of uremic waste products and
inadequate dialysis.
 Hype rtension. Hypertension due to sodium and water retention and the
malfunction of the renin-angiotensin-aldosterone system.
  Ane mia. Anemia due to decreased erythropoietin production decreased RBC
lifespan, bleeding in the GI tract from irritating toxins and ulcer formation,
and blood loss during hemodialysis.
 Bone disease. Bone disease and metastatic and vascular calcifications due to
retention of phosphorus, low serum calcium levels, abnormal vitamin D
metabolism, and elevated aluminum levels.

Nursing Management

The patient with ESRD requires astute nursing care to avoid the complications
of reduced renal function and the stresses and anxieties of dealing with a life-
threatening illness.

Nursing Assessment

Assessment of a patient with ESRD includes the following:

 Assess fluid status (daily weight, intake and output, skin turgor,
distention of neck veins, vital signs, and respiratory effort).
 Assess nutritional dietary patterns (diet history, food preference, and
calorie counts).
 Assess nutritional status (weight changes, laboratory values).
 Assess understanding of cause of renal failure, its consequences and
its treatment.
 Assess patient’s and family’s responses and reactions to illness and
treatment.
 Assess for signs of hyperkalemia.

Diagnosis

Based on the assessment data, the following nursing diagnoses for a

patient with chronic renal failure were developed:

 Excess fluid volume related to decreased urine output, dietary

excesses, and retention of sodium and water.
 Imbalanced nutrition less than body requirements related
to anorexia, nausea, vomiting, dietary restrictions, and altered oral
mucous membranes.
 Activity intolerance related to fatigue, anemia, retention of waste
products, and dialysis procedure.
 Risk for situational low self-esteem related to dependency, role
changes, changes in body image, and change in sexual function.
Planning & Goals
The goals for a patient with chronic renal failure include:

 Maintenance of ideal body weight without excess fluid.

 Maintenance of adequate nutritional intake.
 Participation in activity within tolerance.
 Improve self-esteem.

Nursing Priorities
1. Maintain homeostasis.
2. Prevent complications.
3. Provide information about disease process/prognosis and treatment
needs.
4. Support adjustment to lifestyle changes.

Nursing Interventions
Nursing care is directed towards the following:

 Fluid status. Assess fluid status and identify potential sources of

imbalance.
 Nutritional intake. Implement a dietary program to ensure proper
nutritional intake within the limits of the treatment regimen.
 Independence. Promote positive feelings by encouraging increased
self-care and greater independence.
 Protein. Promote intake of high-biologic –value protein foods: eggs,
dairy products, meats.
 Medications. Alter schedule of medications so that they are not
given immediately before meals.
 Rest. Encourage alternating activity with rest.

Evaluation
A successful nursing care plan has achieved the following:

 Maintained ideal body weight without excess fluid.

 Maintained adequate nutritional intake.
 Participated in activity within tolerance.
  Improved self-esteem.

Discharge and Home Care Guidelines

The nurse should promote home and self-care to increase the esteem of
the patient.

 Vascular access care. The patient should be taught how to check

the vascular access device for patency and appropriate precautions,
such as avoiding venipuncture and blood pressure measurements on
the arm with the access device.
 Problems to report. The patient and the family need to know what
problems to report: nausea, vomiting, change in usual urine output,
ammonia odor on breath, muscle weakness, diarrhea, abdominal
cramps, clotted fistula or graft, and signs of infection.
 Follow-up. The importance of follow-up examinations and
treatment is stressed to the patient and family because of changing
physical status, renal function, and dialysis requirements.
 Home care referral. Referral for home care gives the nurse an
opportunity to assess the patient’s environment and emotional status
and the coping strategies used by the patient and family.

Documentation Guidelines
The documentation in a patient with chronic renal failure should focus on
the following:

 Existing conditions contributing to and degree of fluid retention.

 I&O and fluid balance.
 Results of laboratory tests.
 Caloric intake.
 Individual cultural or religious restrictions and personal preferences.
 Level of activity.
 Plan of care.
 Teaching plan.
 Response to interventions, teaching, and actions performed.
 Attainment or progress toward desired outcomes.
 Modifications to plan of care.
 Long term needs.
 CRITICAL CARE M ANAGEM ENT FOR PATIENT W ITH DIABETIC
KETOACIDOSIS (DKA) NCM 118 LECTURE
Prepared by: Ryan Jay L. Yalung

INTRODUCTION

Ketoacidosis is a metabolic state associated with pathologically high serum and urine

concentrations of ketone bodies, namely acetone, acetoacetate, and beta-hydroxybutyrate. During

catabolic states, fatty acids are metabolized to ketone bodies, which can be readily utilized for

fuel by individual cells in the body. Of the three major ketone bodies, acetoacetic acid is the only

true ketoacid chemically, while beta-hydroxybutyric acid is a hydroxy acid, and acetone is a true

ketone. Figure 1 shows the schematic of ketogenesis where the fatty acids generated after

lipolysis in the adipose tissues enter the hepatocytes via the bloodstream and undergo beta-

oxidation to form the various ketone bodies. This biochemical cascade is stimulated by the

combination of low insulin levels and high glucagon levels (i.e., a low insulin/glucagon ratio).

Low insulin levels, most often secondary to absolute or relative hypoglycemia as with fasting,

activate hormone-sensitive lipase, which is responsible for the breakdown of triglycerides to free

fatty acid and glycerol.

The clinically relevant ketoacidoses to be discussed include diabetic ketoacidosis (DKA),

alcoholic ketoacidosis (AKA), and starvation ketoacidosis. DKA is a potentially life-threatening

complication of uncontrolled diabetes mellitus if not recognized and treated early. It typically

occurs in the setting of hyperglycemia with relative or absolute insulin deficiency. The paucity of

insulin causes unopposed lipolysis and oxidation of free fatty acids, resulting in ketone body

production and subsequent increased anion gap metabolic acidosis. Alcoholic ketoacidosis

occurs in patients with chronic alcohol abuse, liver disease, and acute alcohol ingestion.
Starvation ketoacidosis occurs after the body is deprived of glucose as the primary source of

energy for a prolonged time, and fatty acids replace glucose as the major metabolic fuel.

Nursing Diagnosis
 Nausea, vomiting
 Abdominal pain
 Excess thirst
 Dyspnea
 Malaise
 Excessive urination
 Confusion
 Elevated blood sugar levels
 Fruit scented breath
 High levels of ketones in the urine

Causes
DKA can occur in patients with diabetes mellitus, most frequently associated with

relative insulin deficiency. This may be caused by precipitating physiologic stress or in some

cases, may be the initial clinical presentation in patients with previously undiagnosed diabetes.

Some of the more common risk factors that can precipitate the development of extreme

hyperglycemia and subsequent ketoacidosis are infection, non-adherence to insulin therapy,

acute major illnesses like myocardial infarction, sepsis, pancreatitis, stress, trauma, and the use

of certain medications, such as glucocorticoids or atypical antipsychotic agents which have the

potential to affect carbohydrate metabolism.

AKA occurs in patients with chronic alcohol abuse. Patients can have a long-standing

history of alcohol use and may also present following binges. Acetic acid is a product of the

metabolism of alcohol and also a substrate for ketogenesis. The conversion to acetyl CoA and
subsequent entry into various pathways or cycles, one of which is the ketogenesis pathway is

determined by the availability of insulin in proportion to the counter-regulatory hormones, which

are discussed in more detail below.

Under normal conditions, cells rely on free blood glucose as the primary energy source,

which is regulated with insulin, glucagon, and somatostatin. As the name implies, starvation

ketoacidosis is a bodily response to prolonged fasting hypoglycemia, which decreases insulin

secretion, shunting the biochemistry towards lipolysis and the oxidation of the by-product fatty

acids to ensure a fuel source for the body.

Risk Factors
DKA occurs more frequently with type 1 diabetes, although 10% to 30% of cases occur

in patients with type 2 diabetes, in situations of extreme physiologic stress or acute illness.

According to the morbidity and mortality review of the CDC, diabetes itself is one of the most

common chronic conditions in the world and affects an estimated 30 million people in the United

States. Age-adjusted DKA hospitalization rates were on the downward trend in the 2000s but

have steadily been increasing from thereafter till the mid-2010s at an average annual rate of

6.3%, while there has been a decline in in-hospital case-fatality rates during this period.

For AKA, the prevalence correlates with the incidence of alcohol abuse without racial or

gender differences in incidence. It can occur at any age and mainly in chronic alcoholics but

rarely in binge drinkers.

For starvation ketosis, mild ketosis generally develops after a 12- to 14-hour fast. If there

is no food source, as in the case of extreme socio-economic deprivation or eating disorders, this

will cause the body’s biochemistry to transform from ketosis to ketoacidosis progressively, as
described below. It can be seen in cachexia due to underlying malignancy, patients with

postoperative or post-radiation dysphagia, and prolonged poor oral intake.

Assessment
Patients with DKA may have a myriad of symptoms on presentation, usually within

several hours of the inciting event. Symptoms of hyperglycemia are common, including polyuria,

polydipsia, and sometimes more severe presentations include unintentional weight loss,

vomiting, weakness, and mentation changes. Dehydration and metabolic abnormalities worsen

with progressive uncontrolled osmolar stress, which can lead to lethargy, obtundation, and may

even cause respiratory failure, coma, and death. Abdominal pain is also a common complaint in

DKA. AKA patients usually present with abdominal pain and vomiting after abruptly stopping

alcohol.

On physical exam, most of the patients with ketoacidoses present with features of

hypovolemia from gastrointestinal or renal fluid and electrolyte losses. In severe cases, patients

may be hypotensive and in frank shock. They may have a rapid and deep respiratory effort as a

compensatory mechanism, known as Kussmaul breathing. They may have a distinct fruity odor

to their breath, mainly because of acetone production. There may be neurological deficits in

DKA, but less often in AKA. AKA patients may have signs of withdrawal like hypertension and

tachycardia. There are signs of muscle wasting in patients with starvation ketoacidosis like poor

muscle mass, minimal body fat, obvious bony prominences, temporal wasting, tooth decay,

sparse, thin, dry hair and low blood pressure, pulse, and temperature.

Evaluation
 The initial laboratory evaluation of a patient with suspected DKA includes blood levels

of glucose, ketones, blood urea nitrogen, creatinine, electrolytes, calculated anion gap, arterial

blood gases, osmolality, complete blood count with differential, blood cultures and urine studies

including ketones, urinalysis, urine culture, chest radiograph, and an electrocardiogram.

Hyperglycemia is the typical finding at presentation with DKA, but patients can present with a

range of plasma glucose values. Although ketone levels are generally elevated in DKA, a

negative measurement initially does not exclude the diagnosis because ketone laboratory

measurements often use the nitroprusside reaction, which only estimates acetoacetate and

acetone levels that may not be elevated initially as beta-hydroxybutyrate is the major ketone that

is elevated. The anion-gap is elevated, as mentioned above because ketones are unmeasured

anions. Leukocytosis may indicate an infectious pathology as the trigger and cultures are sent

from blood, urine, or other samples as clinically indicated. Serum sodium is usually relatively

low because of shifts of solvent (water) from the intracellular to extracellular spaces because of

the osmotic pull of hyperglycemia, and hence, normal or elevated serum sodium is indicative of

severe volume depletion. Serum potassium levels may be elevated due to shifts from the

intracellular compartment for exchange with acids in the absence of insulin and normal or low

potassium, indicating an overall depleted body store and subsequent need for correction before

initiation of insulin therapy.

In AKA, transaminitis, and hyperbilirubinemia due to concurrent alcoholic hepatitis may

also be present. The alcohol level itself need not be elevated as the more severe ketoacidosis

is seen once the level falls, and the counter-regulatory response begins and shunts the

metabolism towards lipolysis. Hypokalemia and increased anion-gap are usually seen with

similar mechanisms to those seen in DKA.

 Hypomagnesemia and hypophosphatemia are common problems seen on lab evaluation

due to decreased dietary intake and increased losses. As mentioned above, the direct

measurement of serum beta-hydroxybutyrate is more sensitive and specific than the

measurement of urine ketones. Starvation ketoacidoses patients may again have multiple

electrolyte abnormalities due to chronic malnutrition, along with vitamin deficiencies. The pH

may not be as low as in DKA or AKA, and the glucose levels may be relatively normal.

Medical Management
After initial stabilization of circulation, airway, and breathing as a priority, specific

treatment of DKA requires correction of hyperglycemia with intravenous insulin, frequent

monitoring, and replacement of electrolytes, mainly potassium, correction of hypovolemia with

intravenous fluids, and correction of acidosis. Given the potential severity and the need for

frequent monitoring for intravenous insulin therapy and possible arrhythmias, patients may be

admitted to the intensive care unit. Blood glucose levels and electrolytes should be monitored on

an hourly basis during the initial phase of management.

Aggressive volume resuscitation with isotonic saline infusion is recommended in the

initial management of DKA. Volume expansion not only corrects the hemodynamic instability

but also improves insulin sensitivity and reduces counter-regulatory hormone levels. After

starting with isotonic saline, the subsequent options can be decided on the serum sodium levels

that are corrected for the level of hyperglycemia. Normal or high serum sodium levels warrant

replacement with hypotonic saline, and low sodium levels warrant continuation of the isotonic

saline. This fluid has to be supplemented with dextrose once the level reaches around 200 to 250

mg/dl. Along with fluids, an intravenous infusion of regular insulin has to be initiated to

maintain the blood glucose level between 150 to 200 mg/dl and until the high anion-gap acidosis
is resolved in DKA. Like mentioned above, potassium levels are usually high because of the

transcellular shifts due to the acidosis and the lack of insulin. When the potassium levels are low,

this means that the total body potassium is low. Hence, insulin therapy should be postponed until

at least the level of serum potassium is greater than 3.3 mEq/L. Otherwise, a further drop in

levels would put the patient at risk for cardiac arrhythmias. In the 3.3 to 5 mEq/L; range,

supplementation should be added in the maintenance fluids to target a steady 4.0 to 5.0 mEq/L

range, and if higher than that, insulin and intravenous fluids alone can be started with just the

frequent monitoring of the serum potassium level. The treatment of the acidosis itself is more

controversial. Treatment with sodium bicarbonate therapy is controversial. It has been studied

and found to provide no added benefit when the arterial blood pH is greater than 6.9 and may be

associated with more harm.[5] A 2011 systematic review found that bicarbonate administration

worsened ketonemia. Several studies have found higher potassium requirements in patients

receiving bicarbonate. Studies in children have observed a possible association between

bicarbonate therapy and cerebral edema.[6]

AKA typically responds to treatment with intravenous saline and intravenous glucose,

with rapid clearance of the associated ketones due to a reduction in counter-regulatory hormones

and the induction of endogenous insulin. Like in DKA, this is the first step in management

because of the need for correction the hypovolemia/shock. Thiamine replacement is important in

alcohol-related presentations, including intoxication, withdrawal, and ketoacidosis, and should

be initially done parenterally and after that maintained orally. Electrolyte replacement is critical.

Potassium losses that occur through gastrointestinal (GI) or renal losses should be monitored and

replaced closely as glucose in the replacement fluid induces endogenous insulin, which in

turn drives the extracellular potassium inside the cells. Also of paramount importance is
monitoring and replacing the magnesium and phosphate levels, which are usually low in both

chronic alcoholism and prolonged dietary deprivation as in starvation.

The treatment of starvation ketoacidosis is similar to AKA. Patients need to be monitored

for refeeding syndrome, which is associated with electrolyte abnormalities seen when aggressive

feeding is started in an individual starved for a prolonged time. The resultant insulin secreted

causes significant transcellular shifts, and hence, similar to AKA, monitoring and replacing

potassium, phosphate, and magnesium is very important.

Nursing Management
 Monitor vitals
 Check blood sugars and treat with insulin as ordered
 Start two large-bore IVs
 Administer fluids as recommended
 Check electrolytes as potassium levels will drop with insulin treatment
 Check renal function
 Assess mental status
 Look for signs of infection (a common cause of DKA)
 Educate the patient on the importance of compliance with diabetic medications
 Educate the patient on the importance of follow up
 Check urine output
 Encourage patient to quit smoking and abstain from alcohol
 Encourage a healthy diet
 Ask the patient to wear an ID bracelet signifying that he or she has had a DKA episode
 Check urine and blood cultures
 Listen to the lungs for rales and crackles

When To Refer to Physician?

 Altered mental status
  Dyspnea
 Respiratory distress
 Abnormal vital signs
 Unresponsive

Discharge Planning
Diabetes, once diagnosed, is mostly managed with changes in diet, lifestyle, and

medication adherence. The goal is to prevent high glucose levels, which helps prevent diabetic

complications. To prevent the complications of diabetes like ketoacidosis, the condition is best

managed by an interprofessional team that includes the nurse practitioner, pharmacist, primary

care provider, and an endocrinologist; all these clinicians should educate the patient on glucose

control at every opportunity.

The diabetic nurse should follow all outpatients to ensure medication compliance,

followup with clinicians, and adopting a positive lifestyle. Further, the nurse should teach the

patient how to monitor home blood glucose and the importance of careful monitoring of blood

sugars during infection, stress, or trauma. The physical therapist should be involved in educating

the patient on exercise and the importance of maintaining healthy body weight.

The social worker should be involved to ensure that the patient has the support services

and financial assistance to undergo treatment. The members of the interprofessional team should

communicate to ensure that the patient is receiving the optimal standard of care.

Please take note of this!

The American Association of Clinical Endocrinologists and the American College of

Endocrinology have reviewed reported cases of DKA in patients taking SGLT2 inhibitors. This
association is weak; however, if DKA develops in patients taking SGLT2 inhibitors, stop the

drug immediately, and proceed with traditional DKA treatment protocols. When DKA is found

in patients using SGLT2 inhibitors, it is often “euglycemic” DKA, defined as glucose less than

250. Therefore, rather than relying on the presence of hyperglycemia, close attention to signs and

symptoms of DKA is needed.

In May 2015, the US Food and Drug Administration (FDA) issued a warning [B] that treatment

with sodium-glucose transporter-2 (SGLT2) inhibitors, which include canagliflozin,

dapagliflozin, and empagliflozin, may increase the risk of diabetic ketoacidosis (DKA) in

patients with diabetes mellitus. The FDA Adverse Event Reporting System database identified

20 cases of DKA in patients treated with SGLT2 inhibitors from March 2013 to June 2014.

References
Newcomer JW. Second-generation (atypical) antipsychotics and metabolic effects: a
comprehensive literature review. CNS Drugs. 2005;19 Suppl 1:1-93.
2.
Nyenwe EA, Kitabchi AE. The evolution of diabetic ketoacidosis: An update of its
etiology, pathogenesis and management. Metabolism. 2016 Apr;65(4):507-21.
3.
Benoit SR, Zhang Y, Geiss LS, Gregg EW, Albright A. Trends in Diabetic Ketoacidosis
Hospitalizations and In-Hospital Mortality - United States, 2000-2014. MMWR Morb
Mortal Wkly Rep. 2018 Mar 30;67(12):362-365.
4.
Howard RD, Bokhari SRA. StatPearls [Internet]. StatPearls Publishing; Treasure Island
(FL): Sep 6, 2022. Alcoholic Ketoacidosis.
5.
Allison MG, McCurdy MT. Alcoholic metabolic emergencies. Emerg Med Clin North
Am. 2014 May;32(2):293-301.
6.
Krebs HA, Freedland RA, Hems R, Stubbs M. Inhibition of hepatic gluconeogenesis by
ethanol. Biochem J. 1969 Mar;112(1):117-24.
7.
Chua HR, Schneider A, Bellomo R. Bicarbonate in diabetic ketoacidosis - a systematic
review. Ann Intensive Care. 2011 Jul 06;1(1):23.
8.
Wilson JF. In clinic. Diabetic ketoacidosis. Ann Intern Med. 2010 Jan 05;152(1):ITC1-1,
ITC1-2, ITC1-3,ITC1-4, ITC1-5, ITC1-6, ITC1-7, ITC1-8, ITC1-9, ITC1-10, ITC1-11,
ITC1-12, ITC1-13, ITC1-14, ITC1-15, table of contents; quiz ITC1-16.
9.
Handelsman Y, Henry RR, Bloomgarden ZT, Dagogo-Jack S, DeFronzo RA, Einhorn D,
Ferrannini E, Fonseca VA, Garber AJ, Grunberger G, LeRoith D, Umpierrez GE, Weir
MR. AMERICAN ASSOCIATION OF CLINICAL ENDOCRINOLOGISTS AND
AMERICAN COLLEGE OF ENDOCRINOLOGY POSITION STATEMENT ON THE
ASSOCIATION OF SGLT-2 INHIBITORS AND DIABETIC KETOACIDOSIS. Endocr
Pract. 2016 Jun;22(6):753-62.
10.
Seckold R, Fisher E, de Bock M, King BR, Smart CE. The ups and downs of low-
carbohydrate diets in the management of Type 1 diabetes: a review of clinical
outcomes. Diabet Med. 2019 Mar;36(3):326-334.
11.
George JT, Mishra AK, Iyadurai R. Correlation between the outcomes and severity of
diabetic ketoacidosis: A retrospective pilot study. J Family Med Prim Care. 2018 Jul-
Aug;7(4):787-790.
Emergency Nursing
Clinical Signs of Pain 2

 Vocalization  Pale mucous membranes

 Depression  Aggression
 Anorexia  Abnormal postures
 Tachypnea  Hypersalivation
 Tachycardia  Dilated pupils
 Abnormal blood pressure
Abdominal Pain 3

 Classic “praying” or “play bowing” position

 Hypersalivation
 Inability to lay down or sleep
Untreated Pain 4

 Causes stress
 Triggers harmful physiological changes that prolong
recovery
 Signs not always obvious
 Monitor for absence of normal behavior
DIC 5

 Definition
 A syndrome
 The natural balance between clot formation and clot
prevention/resolution is altered
DIC 6

 Consequences
 Massive activation of coagulation
 Coagulation overwhelms body’s normal regulatory function
 Systemic clot formation begins on a widespread scale
 Clot formations will set up multiple-organ microthrombosis
 Subsequent multiple organ failure
DIC 7

 Causes
 Vascular injury
 Severe trauma
 Severe inflammation
 Sepsis
 Toxins
 Poor perfusion
DIC 8

 Pathogenesis
 Patient commonly moves from a hypercoagulable to a
hypocoagulable state
 Die from thrombotic or hemorrhagic episodes
DIC 9

 Common physical examination findings

 Petechia
 Ecchymosis
 Cold extremities
 Abnormal mentation
 Abnormal body temperature
 Increased respiratory effort
Treatment of DIC 10

 Primary goal
 Remove the stimulus initiating intravascular coagulation
 Treat the primary disease
Treatment of DIC 11

 Secondary goal
 Prevent secondary complications
 Maintain organ perfusion
 Fluids
 Blood products
 Anticoagulants
Shock 12

 Definition
 Poor blood flow creating impaired oxygen delivery to the
tissues
Categories of Shock 13

 Compensatory or hyperdynamic
 Earliest phase of shock
 Clinical signs
 Increased heart rate and respiratory rate
 Rapid capillary refill time
 Brick red mucous membranes
 Bounding pulses
Categories of Shock 14

 Uncompensated or hypodynamic shock

 Second phase of shock
 Blood flow is shunted vital organs (brain, heart) at the
expense of other tissues
 Clinical signs
 Weak pulses
 Rapid heart rate
 Increased capillary refill time
 Pale mucous membranes
 Hypothermia
 Dull mentation
Categories of Shock 15

 Shock can be further divided based on underlying cause

 Hypovolemic shock
 Distributive shock
 Cardiogenic shock
 Septic shock
Hypovolemic Shock 16

 Most common form of shock

 Primary perfusion failure
 Results from a reduction in circulating blood volume
 Bleeding
 Dehydration
 Effusive fluid loss
Distributive Shock 17

 Maldistribution of blood flow associated with

vasodilation
 Consequent decrease in effective blood volume
 Regardless of intravascular volume or cardiac output
 Common causes
 Trauma
 Heatstroke
 Envenomation
 Anaphylaxis
Cardiogenic Shock 18

 Associated with decreased cardiac output

 Can occur from heart failure
 Cardiomyopathy
 Valvular disease
 Cardiac arrhythmias
Septic Shock 19

 Caused by massive systemic infection or primary

infectious diseases
 Opportunistic infections can also trigger septic shock
 Typically associated with severe tissue damage
 Trauma
 Heatstroke
 Envenomations
 Pancreatitis
SIRS 20

 Systemic inflammatory response syndrome

 Parallels septic shock
 Triggered by systemic inflammation
SIRS 21

 Similar to shock in that there is an early hyperdynamic

phase followed by uncompensated or hypodynamic
phase
 Clinical signs
 Abnormal temperature fluctuations
 Depression
 Tachypnea
 DIC
SIRS 22

 Primary treatment
 Oxygen therapy
 Aggressive fluid therapy
 “Shock” doses
 90 ml/kg/hr dog
 45-60 ml/kg/hr cat
 Fluid administration goal oriented!
 Correction of underlying problem
Reperfusion Injury 23

 Cellular injury that develops as blood flow returns to an

area or tissue previously deprived of perfusion
 Poor perfusion causes oxygen-starved tissues to
develop an anaerobic metabolism and become depleted
of cellular energy stores
 These conditions alter certain enzyme systems, which
destabilize white blood cell membranes
Reperfusion Injury 24

 Once perfusion is restored, altered enzyme systems

generate harmful molecules called oxygen-free radicals
 Simultaneously, membrane-damaged white blood cells
release inflammatory mediators that contribute to a
reactive environment
 Oxygen-free radicals and inflammatory mediators cause
inflammation and vessel injury leading to thrombosis
and edema
Vessel Injury 25

 Leads to thrombosis and edema

 DIC, SIRS, and multi-organ dysfunction can develop
Liver Failure/ Hepatic Failure
 LIVER FAILURE

Liver failure is an uncommon condition

in which rapid deterioration of liver
function results in coagulopathy and
alteration in the mental
status( encephalopathy ).

Liver failure indicates that liver has

sustained injury.
TYPES OF LIVER FAILURE

FULMINANT
Non fulminant
HEPATIC
hepatic
FAILURE
failure
• Encephalopathy • Encephalopathy
starts within 8 starts between
weeks 8 to 26 weeks
ACUTE LIVER FAILURE

Acute liver failure (ALF) is

a rare condition
characterized by the abrupt
onset of severe liver injury.
 ALF
• Acute liver failure is loss of liver function
that occurs rapidly — in days or weeks —
usually in a person who has no pre-
existing liver disease .
• It's a medical emergency that requires
hospitalization .
INCIDENCE
• In developed country incidence is 10
cases per million people per year.
• it accounts for 6% of all deaths due to
liver disease.
• It is more common in women than in
men, and more common in white people
than in other races.
ETIOLOGY OF ALF

• DRUG TOXIN
VIRAL INDUCED RELATED
HEPATITIS HEPATOTOX HEPATOTOX
ICITY ICITY

VASCULAR METABOLIC
CAUSES CAUSES
VIRAL HEPATITIS

Virus hepatitis may lead to hepatic failure.

Hepatitis A and B Accounts for most of the
cases.
Atypical causes of viral hepatitis and
fulminant hepatic failure include the following:
Cytomegalovirus, Herpes simplex virus,
paramyxovirus, Epstein-Barr virus
DRUG INDUCED HEPATOTOXICITY
• Acetaminophen is the main drug for these
type of hepatotoxicity.
• Acetaminophen (also known as paracetamol )
may lead to liver failure as a result of intentional
or accidental overdose.
• Some kind of antibiotics, antidepressants,
anaesthetic agents, Salicylates are also
associated with hepatotoxicity.
TOXIN RELATED HEAPTOTOXICITY
Amanita phalloides,

mushroom toxin.

Cyanobacteria toxin .

Organic solvents (eg, carbon tetrachloride).

Yellow phosphorus.
AMNITA PHALLOIDES
VAhepatitis./
SICscUhLemShock
AiRc CAU•Sblood
insufficient LEiSver
flow
injury liver caused by

• Occlusion of
Budd chairi
hepatic veins that
syndrome . drains liver

Portal vein • Blockage or

thrombosis. narrowing of the portal
vein.
METABOLIC CAUSES
Alpha1-antitrypsin . (shape and blockage )

Fructose intolerance. (Def. of aldolase B which

results in inability to convert fructose 1 phosphate
into dihydroxyacetone and glyceraldehyde. )

Galactosemia (Decreased liver enzyme to break

down )
Reye syndrome. (fatty liver+ encephalopathy )
Wilson disease. (copper accumulation )
MALIGNANCIES
• primary liver tumour
(hepatocellular carcinoma).
• Secondary tumour includes
hepatic metastasis or breast, lung
cancer .
C/M OF
ALF
 Hepatic encephalopathy (mental
confusion, difficulty concentrating and
disorientation)
 Sudden jaundice .
 Pain and tenderness in the upper right side
of the stomach.
 Nausea.
 Vomiting.
 Melena.
• Ascites (accumulation of fluid in
the stomach)
• Ankle Edema (accumulation of fluid in the
legs, ankles and feet)
• Feeling ill (Malaise).
• Drowsiness.
• Muscle tremors.
• Bleeding easily
• Cerebral oedema
• Coma
• Brain herniation.
• Hypotension.
• Tachycardia.
• Hematemesis.
DIAGNOSTIC EVALUATION
• History collection.
• Physical examination.
• CBC.
• Prothrombin time (PT) . (9.5-13.5 Seconds )
• SGOT , SGPT.
• Serum billirubin level, Serum ammonia level.
• ABG.
• Serum Creatinine level,
• Serum free copper
• Ceruloplasmin level. (20-38mg/dl)(wilson diases)
• Blood cultures: For patients with
suspected
infection.
• Viral serology: hepatitis A
immunoglobulin M virus
surface antigen (HBsAg).
(IgM), hepatitis B
• Drug screening.
• Electroencephalography(EEG)
• Intracranial pressure monitoring.
• Percutaneous (contraindicated in
presence of coagulopathy) or transjugular
liver biopsy.
• Autoimmune markers:Autoimmune
markers autoimmune hepatitis
(for
A.diagnosis):
Antinuclear antibody (ANA).
B. Anti-smooth muscle antibody (ASMA).
MANAGEMENT OF ALF

Treatment of acute liver failure consists

of Drugs and liver transplantation.
Pharmacological
management includes certain
antidotes to reverse the effects of ALF
and various medications to reduce
ICP.
Antidotes neutralize toxic agents or
counteract any form of poisoning.
PHARAMACOLOGICAL INTERVENTION
Penicillin G.

Activated charcoal.

N-Acetylcysteine.

Osmotic diuretics.

Barbiturate.

Benzodiazepine.

Anaesthetic agents.
 PENICILLIN G
• Intravenous Penicillin G is the drug of
choice for the treatment of Mushroom
Poisoning from Amanita Phalloides.
ACTIVATED CHARCOL
• Patients who have recently ingested A.
Phalloides activated charcoal may bind
the toxin and prevent absorption.
ACTIVATED CHARCOAL
EFFECT OF ACTIVATED CHARCOAL
N-Acectylcycteine
• It is the drug of choice in
acetaminophen overdose.
•
OSMOTIC DIUERETICS
• Intracranial hypertension in acute liver
failure managed by osmotic diuretics such
as Mannitol.
• Mannitol decreases cerebral Edema.
BARBITURATE
• Pentobarbital are used when severe
intracranial hypertension does not respond
to any measures.
BENZODIAZEPENE
• Midazolam is used for sedation
in mechanically ventilated patients.
ANEASTHATIC AGENTS
• Propofol is a sedative hypnotic used
to reduce cerebral blood flow.
LIVER TRANSPLANTATION

During a liver
When acute transplant, a
liver failure surgeon Liver
can't be removes transplantation
reversed, the patient’s is indicated
only treatment damaged liver for many
may be a and replaces it patients with
liver with a healthy ALF.
transplant. liver .
COMPLICATIONS

Kidney Cerebral
failure. Edema.

Bleeding
Infections.
disorders.
 OTHER INTERVENTIONS
For coagulopathy/ GIT bleeding vitamin K
can be given to treat abnormal PT.

Hypotension should be treated with fluids.

Pulmonary complications
mechanical ventilation may be required.
Head of the patient should be elevated to
30 degree .
Neurological status should be
monitored regularly.
NURSING DIAGNOSIS
• Increased risk of dehydration, electrolytes
and metabolic disturbances related to liver
damage.
• Increased risk of secondary infections due
to impaired immune state , related to liver
dysfunction.
• Increased risk of haematological
complications related to liver dysfunction.
contd
• Changes in neurological
state( Encephalopathy) due to liver
insufficiency.
• Increased risk of
haematological complications related to
liver dysfunction.
• Anxiety related to the symptoms
of disease and fear of the unknown.
NURSING INTERVENTIONS
• Assess, report and record signs and
symptoms and reactions to the treatment.
• Monitor fluids input and output closely,
observe signs of dehydration, secondary
infections, neurological disturbances, Edema
and jaundice.
• Provide adequate diet with high proteins,
carbohydrates and vitamins ( carefully in
encephalopathy) .
Contd.
• Administer antibiotics, antiemetic, vitamins
and other medications as prescribed, monitor
for side effects.
• Monitor for signs of possible bleeding.
• Provide prescribed diet, rest and comfort
measures.
• Provide emotional support to client and his
family , explain all procedure to decrease
anxiety and to obtain cooperation.
PREVENTIVE MEASURES
• Tell doctor about all medicines. Over the
counter and herbal medicines interfere
with the drugs.
• Limit the amount of alcohol.
• Do not have wild mushrooms.
• Get vaccinated for hepatitis.
• Avoid contact with other people blood or
body fluids.
Systemic Inflammatory Response Syndrome (SIRS)
and
Multiple Organ Dysfunction Syndrome (MODS)

Copyright © 2017, Elsevier Inc. All Rights Reserved.

SIRS
• Systemic inflammatory response syndrome (SIRS) is a systemic
inflammatory response to a variety of insults
• Generalized inflammation in organs remote from the initial insult

Copyright © 2017, Elsevier Inc. All Rights Reserved.

SIRS
• Triggers
• Mechanical tissue trauma: burns, crush injuries, surgical procedures
• Abscess formation: intraabdominal, extremities
• Ischemic or necrotic tissue: pancreatitis, vascular disease, MI

Copyright © 2017, Elsevier Inc. All Rights Reserved.

SIRS
• Triggers
• Microbial invasion: bacteria, viruses, fungi
• Endotoxin release: gram-negative bacteria
• Global perfusion deficits: postcardiac resuscitation, shock states
• Regional perfusion deficits: distal perfusion deficits

Copyright © 2017, Elsevier Inc. All Rights Reserved.

MODS
• Multiple organ dysfunction syndrome (MODS) is failure of two or
more organ systems
• Homeostasis cannot be maintained without intervention
• Results from SIRS

Copyright © 2017, Elsevier Inc. All Rights Reserved.

Relationship of Shock, SIRS, and MODS

Copyright © 2017, Elsevier Inc. All Rights Reserved.

Case Study
SIRS (©WavebreakMedia/Thinkstock)

• K.R., a 28-year-old woman, is brought to the ED by her mother with

confusion, fever, and “flu for past week.”
• She has been vomiting for the past 2 days and has noted generalized
edema.
• Vital signs: T 103.5° F , HR 112, R 24,
BP 88/54

Copyright © 2017, Elsevier Inc. All Rights Reserved.

SIRS and MODS
Pathophysiology
• Consequences of inflammatory response
• Release of mediators
• Direct damage to endothelium
• Hypermetabolism
• Increase in vascular permeability
• Activation of coagulation cascade

Copyright © 2017, Elsevier Inc. All Rights Reserved.

SIRS and MODS
Pathophysiology
• Organ and metabolic dysfunction
• Hypotension
• Decreased perfusion
• Formation of microemboli
• Redistribution or shunting of blood

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SIRS and MODS
Pathophysiology
• Respiratory system
• Alveolar edema
• Decrease in surfactant
• Increase in shunt
• V/Q mismatch
• End result: ARDS

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SIRS and MODS
Pathophysiology
• Cardiovascular system
• Myocardial depression and massive vasodilation
• Results in SVR and BP
• Baroreceptors respond to enhance CO
• Albumin and fluid move out of blood vessels

Copyright © 2017, Elsevier Inc. All Rights Reserved.

SIRS and MODS
Pathophysiology
• Neurologic system
• Mental status changes due to hypoxemia, inflammatory mediators, or
impaired perfusion
• Often early sign of MODS

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SIRS and MODS
Pathophysiology
• Renal system
• Acute kidney injury (AKI)
• Hypoperfusion
• Release of mediators
• Activation of renin-angiotensin-aldosterone system
• Nephrotoxic drugs, especially antibiotics

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SIRS and MODS
Pathophysiology
• GI system
• Motility decreased: abdominal distention and paralytic ileus
• Decreased perfusion: risk for ulceration and GI bleeding
• Potential for bacterial translocation

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SIRS and MODS
Pathophysiology
• Hypermetabolic state
• Hyperglycemia-hypoglycemia
• Insulin resistance
• Catabolic state
• Liver dysfunction
• Lactic acidosis

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SIRS and MODS
Pathophysiology
• Hematologic system
• DIC
• Electrolyte imbalances
• Metabolic acidosis

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Case Study
SIRS (©WavebreakMedia/Thinkstock)

• K.R. is admitted to ICU with a possible diagnosis of sepsis.

• Her urine output is amber and only 15 mL/2 hr.
• Chest x-ray shows bilateral infiltrates.
• WBC count and lactic acid are elevated.

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SIRS and MODS
Interprofessional Care
• Prognosis for MODS is poor
• Goal: prevent the progression of SIRS to MODS
• Vigilant assessment and ongoing monitoring to detect early signs of
deterioration or organ dysfunction are critical

Copyright © 2017, Elsevier Inc. All Rights Reserved.

SIRS and MODS
Interprofessional Care
• Interprofessional care for patients with MODS focuses on
• Prevention and treatment of infection
• Maintenance of tissue oxygenation
• Nutritional and metabolic support
• Appropriate support of individual failing organs

Copyright © 2017, Elsevier Inc. All Rights Reserved.

Case Study
SIRS (©WavebreakMedia/Thinkstock)

• K.R. has a urinary catheter inserted as well as a central venous

catheter.
• Her doctor talks with her mother about the possibility of mechanical
ventilation.
• K.R.’s mother asks why she is so sick and what can be done for her.

Copyright © 2017, Elsevier Inc. All Rights Reserved.

SIRS and MODS
Interprofessional Care
• Prevention and treatment of infection
• Aggressive infection control strategies to decrease risk for nosocomial
infection
• Strict asepsis
• Assess need for invasive lines
• Once an infection is suspected, institute interventions to control source

Copyright © 2017, Elsevier Inc. All Rights Reserved.

SIRS and MODS
Interprofessional Care
• Maintenance of tissue oxygenation
• Decrease O2 demand and increase O2 delivery
• Sedation
• Mechanical ventilation
• Analgesia
• Rest

Copyright © 2017, Elsevier Inc. All Rights Reserved.

SIRS and MODS
Interprofessional Care
• Nutritional and metabolic needs
• Goal of nutritional support: preserve organ function
• Total energy expenditure is often increased 1.5 to 2.0 times

Copyright © 2017, Elsevier Inc. All Rights Reserved.

SIRS and MODS
Interprofessional Care
• Nutritional and metabolic needs
• Use of the enteral route is preferred to parenteral nutrition
• Monitor plasma transferrin and prealbumin levels to assess hepatic protein
synthesis
• Provide glycemic control

Copyright © 2017, Elsevier Inc. All Rights Reserved.

SIRS and MODS
Interprofessional Care
• Nutritional and metabolic needs
• Use of the enteral route is preferred to parenteral nutrition
• Monitor plasma transferrin and prealbumin levels to assess hepatic protein
synthesis
• Provide glycemic control

Copyright © 2017, Elsevier Inc. All Rights Reserved.

SIRS and MODS
Interprofessional Care
• Support of failing organs
• ARDS: aggressive O2 therapy and mechanical ventilation
• DIC: appropriate blood products
• Renal failure: continuous renal replacement therapy or dialysis

Copyright © 2017, Elsevier Inc. All Rights Reserved.

 Audience Response Question
A patient with a history of alcoholism is admitted to the ICU with
hemorrhage from esophageal varices. Admission VS are BP 84/58
mm Hg, HR 105, and RR 32 breaths/min. The nurse recognizes the
onset of systemic inflammatory response syndrome (SIRS) upon
finding
a. pulmonary edema.
b. cardiac dysrhythmias.
c. absent bowel sounds.
d. decreasing blood pressure.

Copyright © 2017, Elsevier Inc. All Rights Reserved.

 Audience Response Question

A patient admitted to the hospital from a long-term care facility

appears to be in the late stage of shock with systemic inflammatory
response syndrome (SIRS). Which order implemented by the nurse has
the highest priority?
a. Insert an indwelling urinary catheter.
b. Insert two large-bore intravenous catheters.
c. Administer 0.9% normal saline at 100 mL/hr.
d. Administer 100% oxygen by non-rebreather mask.

Copyright © 2017, Elsevier Inc. All Rights Reserved.

PANCREATITIS
 OBJECTIVES

 Define acute pancreatitis

 Etiological factors of pancreatitis
 Pathophysiology of acute pancreatitis
 Enlist the clinical manifestations
 Identify the complication
 Diagnostic evaluation
 Discuss the treatment modalities of acute pancreatitis
 Surgical management of acute pancreatitis
 Chronic pancreatitis
 Clinical manifestations of chronic pancreatitis
 Diagnostic evaluation of chronic pancreatitis
 Management of chronic pancreatitis
 Preventive and health promotion measures for pancreatitis
REVIEW OF ANATOMY AND PHYSIOLOGY
 FUNCTIONS
EXOCRINE : ENDOCRINE:

Pancreatic juice Isets of langerhans

Amylase Alpha cells: Glucagon
Lipase (20%)
Beta cells: Insulin
Trypsin
(75%)
Chymotripsin
Gamma cells :
Carboxypeptidase Somatostatin
Polypeptide
 MEANING
 Acute pancreatitis is an acute inflammation of the
pancreas .
 The degree of inflammation varies from mild
edema to severe haemorrhagic necrosis .
 Acute pancreatitis is common in middle aged men
and women
 CAUSES

Two main causes for pancreatitis are

 Gallstones (38%)
 Alcohol (36%)
Other, less common causes of acute pancreatitis
include
 Trauma (postsurgical, abdominal)
 Viral infections mumps
 Coxsackievirus B, HIV
 Penetrating duodenal ulcer cysts
 CAUSES
 Metabolic disorders
 Hyperparathyroidism
 Hyperlipidemia
 Renal failure
 Vascular diseases.
 Pancreatitis may occur after surgical procedures on
the pancreas, stomach, duodenum or biliary tract.
 CAUSES
 Abscesses
Cystic fibrosis
 Kaposi sarcoma
Certain drugs (corticosteroids, thiazide , diuretics,
oral contraceptives, sulfonamides NSAIDs)
Pancreatitis can also occur after ERCP.
In some cases the cause is unknown (idiopathic)
 PATHOPHYSIOLOGY
Etiological factors

Cause injury to pancreatic cells

Activation of the pancreatic enzymes

Reflux of bile acids into the pancreatic

ducts
Open distended sphincter of Oddi causes reflux
due to blockage
 CLINICAL MANIFESTATION

FEVER
 Rarely exceeds 102 degree F

ABDOMINAL FINDINGS
 Rigidity, tenderness, guarding
 Distension
 Decreased or absent peristalsis
 CLINICAL MANIFESTATION
ABDOMINAL PAIN
 Steady and severe excruciating
 Located in the left upper quadrant or in
the mid epigastrium may radiate to
the back

Worsened by lying supine may be

lessened by flexed knee, curved back
positioning
 CLINICAL MANIFESTATION

VOMITTING
 Varies in severity but is usually
protacted.
 Worsened by ingestion of food
or fluid.
 Does not relieve the pain.
 Usually accompanied by
nausea.
 CLINICAL MANIFESTATION
Cullen’s sign Grey’s turner sign

Bluish discoloration around Bluish discoloration along

the umbilicus the flanks
 COMPLICATION
 Hypotension orSshock from hypovolemia or
hypoalbuminemia
 Leukocytosis, anemia , disseminated intravascular
coagulation from unknown causes
 Atelectasis, pneumonia, pleural effusion, acute
respiratory distress syndrome
 Gastrointestinal bleeding
 COMPLICATION
S
Pancreatic pseudocysts, pancreatic necrosis,
pancreatic abscesses, pancreatic ascites
Oliguria and acute tubular necrosis
Hyperglycemia, hypocalcemia, hyperlipidemia
 DIAGNOSIS

History and physical examination

Liver function tests: elevations commonly seen
Serum trigylycerides
 DIAGNOSIS
• Serum amylase: Levels elevated within a few hours
of disease onset
• Serum lipase: Levels remain elevated up to 7 days
after disease onset
• Serum glucose: Hyperglycaemia of 500 to 900
mg/d
• Serum calcium: Hypocalcaemia from calcium
sequestering in abdomen; hypocalcemia is a poor
prognostic sign
 DIAGNOSIS

 Abdominal ultrasound
Endoscopic ultrasound
 DIAGNOSIS

Magnetic Resonance
Cholangiopancreatography
(MRCP)
 DIAGNOSIS

Endoscopic Retrograde
Cholangiopancreatography
(ERCP)
 COLLABORATIVE CARE
GOALS
1) Relief of pain
2) Prevention or alleviation of shock
3) Reduction of pancreatic secretions
4) Correction of fluid and electrolyte imbalances
5) Prevention and treatment of infections
6) Removal of the precipitating cause
 CONSERVATIVE THERAPY

Focused on primary care:

1) Aggressive hydration
2) Management of metabolic complications
3) Minimization of pancreatic stimulation
 CONSERVATIVE THERAPY

1) Management of pain
IV morphine ( pain medication may be
combine with antispasmodic agents)
 Spasmolytics : Nitroglycerine or
papaverine
2)Supplemental oxygen: To maintain oxygen
saturation > 95%
3) Serum glucose : Monitored for
 CONSERVATIVE THERAPY

If shock present
1) Blood volume replacement
2) Plasma or plasma volume expanders : Dextran
or albumin may be given
3) Fluid and electrolyte: Ringer’s lactate solution
4) Increase vascular resistance with hypotension
: Vasoactive drug such as dopamine
 CONSERVATIVE THERAPY

To Suppress the pancreatic enzymes

1)The patient to be kept in NPO
2) NG suction :
 To reduce vomiting and gastric
distension
 To prevent gastric acid contents from entering into
the duodenum
3) Drugs such as Antacids, PPI, Acetazolamide
 CONSERVATIVE THERAPY

4) Enteral nutrition : For patients who does not resume

oral intake
5) Antibiotic therapy: In patients with acute necrotizing
pancreatitis
6) Endoscopic or CT guided percutaneous aspiration
with gram stain and culture may be performed
 SURGICAL THERAPY
1) Acute pancreatitis related to Gallstone:
ERCP together with endoscopic spinchterotomy
followed by laproscopic cholecystectomy to reduce
potential for recurrence

2) Severe acute pancreatitis:

 Drainage of necrotic fluid collections
 DRUG THERAPY
DRUG MECHANISM OF
Morphine ACTION
Relief of pain
Antispasmodic (e.g diclyclomine) Decrease vagal stimulation , motility,
pancreatic outflow
Carbonic anhydrase Decrease volume and bicarbonate
inhibitor (acetazolamide) concentration of pancreatic secretion

Proton pump inhibitors Decrease acid secretion (HCL

acid stimulate pancreatic activity )
Antacids Neutralization of gastric hydrochloride
acid secretion
 NUTRITIONAL MANAGEMENT
 Initially the patient to kept on NPO to decrease the gastric
acid secretions
 Enteral feeding: Nasojejunal feeding tube
 IV lipids : Blood triglyceride levels are monitored
 When food is allowed, small, frequent feedings are given.
 Carbohydrate rich diet should be given
 Needs to abstain from alcohol
 Supplemental fat-soluble vitamins may be given
 CHRONIC PANCREATITIS

DEFINITION
Chronic pancreatitis (CP) is characterised by
prolongedpancreatic inflammation and fibrosis
leading eventually to destruction of pancreatic
parenchyma and loss of exocrine and endocrine
function
 ETIOLOGY

1) Alcohol abuse
2) Obstruction caused by cholelitiasis
3) Tumour
4) Pseudocyst
 ETIOLOGY

5)Trauma
6)Systemic disease (Systemic lupus
erythematosus)
7)Auto immune pancreatitis
8)Cystic fibrosis
 ETIOLOGY
OBSTRUCTIVE NON OBSTRUCTIVE
PANCREATITIS
PANCREATITI Inflammation and
S
sclerosis mainly in
Inflammation of
the head of pancreas
Sphincter of oddi
associated cholelitiasis
and around the
Cancer of ampulla of pancreatic duct
vater duodenum,
 CLINICAL MANIFESTATION
Abdominal pain :
oEpisode of acute pain and it remains almost
constant
oPain may be locate in the same area as acute
pancreatitis
oDescribe as heavy, gnawing feeling or
sometimes burning and cramplike
 CLINICAL MANIFESTATION

Others include:
Malabsorption with weight loss constipation, mild
jaundice with dark urine, steatorrhea and diabetes
mellitus
Staetorrhea may be voluminous, foul smelling
fatty stools
 Urine and stool may be frothy
 Some abdominal tenderness may be present
 COMPLICATION
S
 Pseudocyst formation
 Bile duct or duodenal obstruction
 Pancreatic ascitis
 Pleural effusion
 Splenic vein thrombosis
 Pseudoaneurysm
 Pancreatic cancer
 DIAGNOSIS

Serum amylase
Serum Lipase
Serum bilirubin
 Alkaline phosphatase
 ESR, mild leucocytosis
ERCP
MRCP
 DIAGNOSIS

 CT, MRI
 Abdominal ultrasound
 Stool sample : Fecal fat content
 Deficiencies of fat soluble vitamin and cobalamin,
glucose intolerance
 Secretin stimulation test
 SURGICAL MANGEMENT

 Pancreaticojejunostomy
Side-to-side anastomosis
of the pancreatic duct to the
jejunum, allows drainage of
the pancreatic secretions
into the jejunum.
 SURGICAL MANGEMENT

Whipple resection
(pancreaticoduodenectomy )
Removal of the head of the pancreas, the
first part of the small intestine (duodenum),
the gallbladder and the bile duct.
 SURGICAL MANGEMENT

Other surgical procedures:

Revision of the sphincter of the ampulla of Vater
Internal drainage of a pancreatic cyst into the
stomach
Insertion of a stent and wide resection or
removal of the pancreas.
 SURGICAL MANGEMENT

Autotransplantation :
Implantation of the pancreatic islet cells

Moving the pancreas to another location within

the abdomen with revised vascular and enteric
anastomosis
 SURGICAL MANGEMENT

Gall bladder disease : The obstruction is treated
by surgery to explore the common duct and remove
the stones; the gallbladder is removed at the same
time.

 Drainage : common bile duct and the pancreatic duct

 A T-tube usually is placed in the common bile duct,

requiring drainage system to collect the bile
 NURSING MANAGEMENT
Health History.
Assess for
 History of gallbladder disease
History of other GI diseases (e.g., peptic ulcer
disease, IBD)
 History of alcohol use: amount and duration
Medications in use: prescription, over the counter,
and herbal preparation
 NURSING MANAGEMENT

 Onset and progression of symptoms such as:

Pain, which is often steady and severe; is located in
the epigastric or umbilical region or may radiate to the
back; worsens when patient is supine; is unrelieved
by vomiting
 Nausea and vomiting
 NURSING MANAGEMENT

Physical Examination.
 Assess for:
 Vital sign indications of hypovolemia: tachycardia,
tachypnea, normal to low blood pressure,
restlessness, and anxiety
 Abdominal rigidity, distention, guarding, and
tenderness to palpation
 NURSING MANAGEMENT

Diminished or absent bowel sounds on

auscultation
Fever : > 102° F
Signs of third spacing: falling urinary output,
decreased skin turgor, dry or sticky mucous
membranes, increased abdominal girth
 PRIORITIZED NURSING DIAGNOSIS

Acute pain related to inflammation, edema,

distension of pancreatic capsule and activation
of pancreatic enzyme

Ineffective breathing pattern related to severe

pain, pulmonary infiltrates , pleural effusion,
atelectasis and elevated diaphragm
 PRIORITIZED NURSING DIAGNOSIS

 Risk for deficient fluid volume related to vomiting,

hyperglycemia, and increased capillary permeability
secondary to acute pancretitis
 Imbalanced nutrition less than body requirement related to
vomiting, NPO status and malabsorption secondary to
pancreatitis

 Impaired skin integrity related to poor nutritional status,

bed rest, multiple drains, and surgical wound
Does mortality occur early or late in acute
pancreatitis?
Abstract:
Several prior studies have suggested that 80% of deaths in acute
pancreatitis occur late as a result of pancreatic infection. Others have
suggested that approximately half of deaths occur early as a result of
multisystem organ failure. The aim of the present study was to
determine the timing of mortality of acute pancreatitis at a large tertiary-
care hospital in the United States.
 CONCLUSION
 Conclusion:
Approximately half of deaths in acute pancreatitis occur
within the first 14 days owing to organ failure and the
remainder of deaths occur later because of complications
associated with necrotizing pancreatitis. Improvement in
mortality in the future will require innovative approaches to
counteract early organ failure and late complications of
necrotizing pancreatitis.
Authors
 Muthoka Mutinga,Adam Rosenbluth,Scott M. Tenner,Robert R. Odze
Gregory T. Sica, Peter A. Bank
 REFERENCES
BOOKS
 Lewis, Driksen, Heikemper, Bucher. Lewis Textbook of
medical surgical nursing- 2nd edition
 Urden D.L StacyM.K Laugh E.M Textbook For Critical
Care Nursing
 Myers/Gulanick, Nursing Care Plans. Nursing Diagnosis
And Interventions 6th edition
 Linda s. Williams, Paula D. Hopper. Textbook of medical
surgical nursing-4th edition
SHOCK
 INTRODUCTION

Cells need two things to function: oxygen and glucose. This allows the
cells to generate energy and do their specific jobs. When cells don’t
receive either of them or both, they stop functioning.
 DEFINITION

Shock is defined as a condition where the tissues in the body don't

receive enough oxygen and nutrients to allow the cells to function.
 CLASSIFICATION
1. Cardiogenic shock- It occurs due to systolic or diastolic dysfunction.
2. Hypovolemic shock- It occurs due to intravascular fluid volume.
3. Obstructive shock- It occurs when there is physical obstruction in blood flow.
4. Distributive shock- (neurogenic, anaphylactic & septic)

•Neurogenic shock- It occurs from trauma that leads

to spinal cord injuries.

•Anaphylactic shock- It is acute life threatening

hypersensitivity reaction to a sensitizing
substance like drug, chemical, vaccine, food etc.

• Septic shock- Also known as blood poisoning,

is a condition caused by infections that lead to bacteria

entering blood.
 ETIOLOGY

• Severe allergic reaction

• Significant blood loss
• Heart failure
• Blood infections
• Dehydration
• Poisoning
• Burns
 PATHOPHYSIOLOGY
CARDIOGENIC SHOCK
STRUCTURAL DEFECTS IN HEART, DYSRHYTHMIAS ETC.

SYSTOLIC & DIASTOLIC DYSFUNCTION

DECREASED CARDIAC OUTPUT & INCREASED PULMONARY PRESSURE

PULMONARY EDEMA

DECREASED CELLULAR OXYGEN SUPPLY

DECREASED TISSUE PERFUSION

 HYPOVOLEMIC SHOCK
DECREASED BLOOD VOLUME DUE TO ACCIDENT, BURN ETC.

DECREASED VENOUS RETURN

DECREASED CARDIAC OUTPUT

DECREASED TISSUE PERFUSION

DECREASED CELLULAR METABOLISM

 NEUROGENIC SHOCK
DISRUPTION OF SYMPATHETIC NERVOUS SYSTEM

VASODILATION

DECREASED BP

DECREASED CARDIAC OUTPUT

DECREASED CELLULAR OXYGEN SUPPLY

DECREASED TISSUE PERFUSION

IMPAIRED CELLULAR METABOLISM

 ANAPHYLACTIC SHOCK
ALLERGEN , DRUG ETC.

ANTIGEN ANTIBODY REACTION

VASODILATION

CAPILLARY PERMEABILITY

SEVERE BRONCHO CONSTRICTION

DECREASED OXYGEN SUPPLY AND

UTILIZATION

INADEQUATE TISSUE PERFUSION

 SEPTIC SHOCK
INFECTION

RELEASE OF
TOXIN

PERIPHERAL VASCULAR EFFECTS MYOCARDIAL

PROBLEMS

ENDOTHELIAL DECREASED
DESTRUCTION CONTRACTILITY

MICROVASCULAR INSUFFICIENCY INADEQUATE BLOOD FLOW

TO TISSUE

INADEQUATE BLOOD FLOW TO THE TISSUE TISSUE HYPOXIA

CELL DEATH
 OBSTRUCTIVE SHOCK
PHYSICAL OBSTRUCTION IN BLOOD FLOW

DECREASED VENOUS RETURN

DECREASED CARDIAC OUTPUT

DECREASED CELLULAR OXYGEN SUPPLY

DECREASED TISSUE PERFUSION

IMPAIRED CELLULAR METABOLISM

 CLINICAL MANIFESTATIONS

• Extremely low blood pressure

• Weakness
• Chest pain
• Weak pulse
• Profuse sweating
• Dizziness
• Moist, clammy skin
• Unconsciousness
• Rapid, shallow breathing
• Feeling anxious, agitated or confused
• Cyanosis
 DIAGNOSTIC EVALUATION

• History collection

• Physical examination

• Blood culture & sensitivity test

• CBC- increased WBC & ESR level

• Arterial blood gas analysis- respiratory alkalosis

• ECG-dysarrthmias

• Echocardiogram-to rule out aortic stenosis and pulmonary

embolism.

• X-ray & CT scan

• Cardiac monitoring-Spo2,pulse,temp,BP are monitored continuously.

• Central venous pressure -fluid loss.

 COMPLICATION
S

• Loss of consciousness
• Respiratory failure
• Coagulation disorder
• Multi organ damage
• Coma
• Death
 MANAGEMENT
I. MEDICAL MANAGEMENT
A. PHARMACOLOGICAL MANAGEMENT
• Crystalloids: ringer’s solution and normal saline
• Inotropic agents: like dopamine , dobutamine and
epinephrine
• Vasodilators : nitroglycerine
• Diuretics : lasilactone, furosemide
• Antibiotics : ciprofloxacin, amoxicillin and clavulanic acid
• Antihistamines : epinephrine used in anaphylactic shock.
• Corticosteroids : dexamethasone
• Sodium bicarbonate :used to treat metabolic acidosis
• Broncodilators : like atropine , aminophylline etc.
• B. NON- PHARMACOLOGICAL MANAGEMENT
• Modified trendelenberg position

• Assessment of vital signs

• Oxygen administration

• Parenteral nutrition support

II. SURGICAL MANAGEMENT

• Wound debridement- in case of chronic infected wound, burns

wound
debridement to be done for fast healing

• Angioplasty-in case of myocardial infarction angioplasty can be

performed

• Tracheostomy
III. NURSING MANAGEMENT

ASSESSMENT
• Continuous monitoring of vital signs should be done.
• Assess Airway, breathing & circulation of the patient.
• Monitor for ABG value
• Check for urine output of the client.
•
• NURSING DIAGNOSIS

• Impaired tissue perfusion related to decrease cardiac output,

decreased venous return
• In effective breathing pattern related to hypoxia, bronchospasm
• Fluid volume deficit related to vomiting hemorrhage
• Acute pain related to myocardial infarction
• Imbalanced nutrition less then body requirement related to
vomiting, low intake of food
SPINAL INJURY
ANATOMY AND PHYSIOLOGY
DEFINITION
Spinal cord injury (SCI) is
damage to the spinal cord that
results in a loss of function such
as mobility or feeling.
TYPES OF SPINAL CORD INJURY

 Complete Spinal Cord Injuries

Complete paraplegia is described as

permanent loss of motor and nerve
function at T1 level or below, resulting in
loss of sensation and movement in the
legs, bowel, bladder, and sexual region.
Arms and hands retain normal function.
INCOMPLETE SPINAL CORD
INJURIES

Anterior cord syndrome

CENTRAL CORD SYNDROME
POSTERIOR CORD SYNDROME
BROWN-SEQUARD SYNDROME
CAUDA EQUINA
SYNDROME
RISK FACTORS

 Men

Young adults and seniors

 People who are active in sports

 People with predisposing conditions

CAUSES:
 Bullet or stab wound

 Traumatic injury

 Electric shock

 Extreme twisting of the middle of the body

 Landing on the head during a sports injury

SIGNS AND SYMPTOMS
CERVICAL (NECK) INJURIES
 Breathing difficulties

 Loss of normal bowel and bladder

control

 Numbness

 Sensory changes

 Spasticity (increased muscle tone)

THORACIC (CHEST LEVEL) INJURIES

 Loss of normal bowel and bladder

control

 Numbness

 Sensory changes

 Spasticity (increased muscle tone)

LUMBAR SACRAL (LOWER BACK)
INJURIES
 Loss of normal bowel and bladder control (you may
have constipation, leakage, and bladder spasms)

 Numbness

 Pain

 Sensory changes

 Weakness and paralysis

ASSESSMENT
DIAGNOSTIC TESTS
 Complete blood count (e.g. Hb, RBC,
WBC)

 Arterial blood gas level

PaO2:85-95 mm of Hg
PaCO2:35-45 mm of Hg
X- RAYS:
COMPUTERIZED TOMOGRAPHY (CT)
SCANS
MAGNETIC RESONANCE
IMAGING (MRI):
MYELOGRAPHY
:
 POSSIBLE COMPLICATIONS

 Blood pressure changes - can be extreme

(autonomic hyperreflexia)
 Chronic kidney disease

 Complications of immobility:

Deep vein thrombosis

Pulmonary infections
Skin breakdown
 Contractures
 Increased risk of urinary tract infections

 Loss of bladder control

 Loss of bowel control

 Loss of sensation

 Loss of sexual functioning (male

impotence)
 Muscle spasticity

 Paralysis of breathing muscles

 Paralysis (paraplegia, quadriplegia)

 Pressure sores

 Shock
MEDICAL MANAGEMENT:
 Whole blood

 NS

 RL

 Hydrocortisone:
Action :
 Nor epinephrine
action: adrenergic drug

Epinephrine

action: α and β adrenergic drug

Dopamine

action: adrenergic, anti shock drug

SURGICAL
MANAGEMENT
NURSING MANAGEMENT:
Impaired physical mobility related to
loss of motor function

 Fluidvolume deficit related to

decrease LOC

 Riskfor injury related to loss of

motor function
 Urinary retention related to level of
injury

 Risk for Impaired skin integrity related to

trauma

 Knowledge deficit regarding the treatment

modalities and current situation.

 Anxiety related to outcome of diseases as

evidenced by poor concentration on
work, isolation from others, rude
DIET
PLAN
REHABILITATION

Cognitive Rehabilitation Therapy

Speech Therapy

Mental Rehabilitation

Physical Exercise

Occupational Therapy
THANK
YOU