Sei sulla pagina 1di 21

KENYA METHODIST

UNIVERSITY
NAIROBI CAMPUS
NAME: GEOFFREY MUSAMBI
IVASHA
ADM NUMBER: BSN-1-1817-1/2014
2nd TRIMESTER 2016

COURSE: TRAUMA AND


EMERGENCY NURSING
CLINICALS
Course Code: NRSG 467
CASE STUDY
SHOCK

1. INTRODUCTION
TENWEK HOSPITAL
Tenwek Hospital is a Christian community committed to excellence in compassionate
healthcare, spiritual ministry, and training for service to the glory of God. Mission
Statement
Tenwek Hospital was founded in 1937 by World Gospel Mission missionaries and has since
grown to be a leading provider of quality healthcare and medical education in Western
Kenya, and one of the largest mission hospitals in Africa. It is a non-profit hospital
functioning under the leadership of Africa Gospel Church in partnership with World Gospel
Mission.
Tenwek is a 300 bed teaching hospital with a wide range of surgical, medical, maternity and
pediatric services. It provides primary health care to 600,000 people within a 32 kilometer
radius and serves as a referral center for a much larger region. General wards range from six
to 17 beds each. Semiprivate rooms with private baths are available. Private isolation rooms,
an eye ward, and an orthopedic ward were added in 1997. Six operating rooms along with a
recovery room provide facilities for a wide range of surgical services. The hospital has both
outpatient and inpatient services required of modern health facility.

Through partnerships with various organizations, long term and visiting physicians
(Facilitated through Samaritans Purse), provide Tenwek patients with expertise in hospital
care, out-patient treatment (Supported through USAID), and HIV/AIDS care through
the PEPFAR program.
Tenwek is also supported by Friends of Tenwek (FOT), a U.S.-based non-profit organization
dedicated to developing key relationships and resources that help Tenwek fulfill its mission.
FOT has raised funds through various organizations and private donors to support the
projects and goals of Tenwek Hospital in addition to keeping those who have visited Tenwek
in the past informed and involved with what's happening at Tenwek today.

Placement report: The case was taken from trauma and emergency/Casualty department
consisting of 7 bed capacity. The unit is staffed with 16 nurses and 4 support staff. 4 nurses
are available during the day and 2 at night. Besides the nursing cadre, the unit also has 1
clinical officer working during the day and one during the night. At times senior medical
officers and emergency doctors are available throughout the day.

Justification for choosing the patient.

The patient was brought to the unit in unconscious state due to shock
She was in critical condition that required stabilization in emergency department

before being transferred to critical care unit for further management.


It is good case to study since due to dynamics of the patient in shock, the outcome
of management depends on aggressiveness before complications/goes into state of
irreversibility.

2. LITERATURE REVIEW
SHOCK
Definition
Shock is defined as a state of cellular and tissue hypoxia due to reduced oxygen
delivery and/or increased oxygen consumption or inadequate oxygen utilization. This most
commonly occurs when there is circulatory failure manifested as hypotension.
Types of Shock with Signs and symptoms
There are 4 main types of shock
a.
b.
c.
d.

Hypovolemic shock
Cardiogenic shock
Distributive shock
Obstructive shock

Hypovolemic Shock
This is majorly caused by reduction in circulating blood volume in the body due to loss of
blood. Its primary cause is hemorrhage (internal and/or external), or loss of fluid from the
circulation. Vomiting and diarrhea are the most common cause in children.With other causes

including burns, environmental exposure and excess urine loss due to diabetic ketoacidosis
and diabetes insipidus. The loss of blood can lead to

A rapid, weak, thready pulse due to decreased blood flow combined with tachycardia

Cool, clammy skin due to vasoconstriction and stimulation of vasoconstriction

Rapid and shallow breathing due to sympathetic nervous system stimulation and
acidosis

Hypothermia due to decreased perfusion and evaporation of sweat

Thirst and dry mouth, due to fluid depletion

Cold, and mottled skin (Livedo reticularis), especially extremities, due to insufficient
perfusion of the skin

Cardiogenic shock
A condition resulting from an inadequate circulation of blood due to primary failure of
the ventricles of the heart to function effectively. There is insufficient perfusion of tissue to
meet the demands for oxygen and nutrients and thus lead to cardiac arrest if not corrected.
It is commonly caused by the failure of the heart to pump effectively. This can be due to
damage to the heart muscle, most often from a large myocardial infarction. Other causes of
cardiogenic shock include dysrhythmias, cardiomyopathy/myocarditis, congestive heart
failure (CHF), contusiocordis, or cardiac valve problems
Symptoms include:

Anxiety, restlessness, altered mental state due to decreased blood flow to the brain
and subsequent hypoxia.

Low blood pressure due to decrease in cardiac output.

A rapid, weak, thready pulse due to decreased circulation combined with tachycardia.

Cool, clammy, and mottled skin (cutis marmorata) due to vasoconstriction and
subsequent hypoperfusion of the skin.

Distended jugular veins due to increased jugular venous pressure.

Oliguria (low urine output) due to inadequate blood flow to the kidneys if the
condition persists.

Rapid and deeper respirations (hyperventilation) due to sympathetic nervous system


stimulation and acidosis.

Fatigue due to hyperventilation and hypoxia.

Absent pulse in fast and abnormal heart rhythms.

Pulmonary edema, involving fluid back-up in the lungs due to insufficient pumping of
the heart.

Distributive Shock
It is a condition in which abnormal distribution of blood flow in the smallest blood vessels
results in inadequate supply of blood to the body's tissues and organs.Distributive shock is
different from the other three categories of shock in that it occurs even though the output of
the heart is at or above a normal level.

Sepsis,
Systemic inflammatory response syndrome (SIRS) due to conditions other than

infection such as pancreatitis, burns or trauma.


Toxic shock syndrome (TSS),
Anaphylaxis (a sudden, severe allergic reaction),
Adrenal insufficiency, reactions to drugs or toxins, heavy metal poisoning,
Hepatic (liver) insufficiency and damage to the central nervous system.

Signs and symptom are same as above in Cardiogenic and hypovolemic shocks.
Obstructive Shock
It is a form of shock associated with physical obstruction of the great vessels or the heart
itself. Causes include

Cardiac tamponade (condition where the fluid accumulates within the pericardium).
Constrictive pericarditis seen in the later stage.

Aortic stenosis (narrowing of aorta wall)


Tension pneumothorax (condition in which the lungs completely collapse).
Massive pulmonary embolism

Pathophysiology
The human body responds to acute hemorrhage by activating the following major physiologic
systems: the hematologic, cardiovascular, renal, and neuroendocrine systems.
The hematologic system responds to an acute severe blood loss by activating the coagulation
cascade and contracting the bleeding vessels (by means of local thromboxane A2 release). In
addition, platelets are activated (also by means of local thromboxane A2 release) and form an
immature clot on the bleeding source. The damaged vessel exposes collagen, which
subsequently causes fibrin deposition and stabilization of the clot. Approximately 24 hours
are needed for complete clot fibrination and mature formation.
The cardiovascular system initially responds to hypovolemic shock by increasing the heart
rate, increasing myocardial contractility, and constricting peripheral blood vessels. This
response occurs secondary to an increased release of norepinephrine and decreased baseline
vagal tone (regulated by the baroreceptors in the carotid arch, aortic arch, left atrium, and
pulmonary vessels). The cardiovascular system also responds by redistributing blood to the
brain, heart, and kidneys and away from skin, muscle, and GI tract.
The renal system responds to hemorrhagic shock by stimulating an increase in renin secretion
from the juxtaglomerular apparatus. Renin converts angiotensinogen to angiotensin I, which
subsequently is converted to angiotensin II by the lungs and liver. Angiotensin II has 2 main
effects, both of which help to reverse hemorrhagic shock, vasoconstriction of arteriolar
smooth muscle, and stimulation of aldosterone secretion by the adrenal cortex. Aldosterone is
responsible for active sodium reabsorption and subsequent water conservation.

The neuroendocrine system responds to hemorrhagic shock by causing an increase in


circulating antidiuretic hormone (ADH). ADH is released from the posterior pituitary gland
in response to a decrease in BP (as detected by baroreceptors) and a decrease in the sodium
concentration (as detected by osmoreceptors). ADH indirectly leads to an increased
reabsorption of water and salt (NaCl) by the distal tubule, the collecting ducts, and the loop of
Henle.

Effect of inadequate perfusion to a cell is described in the cascade below.

Without fluid and blood resuscitation and/or correction of the underlying pathology causing
the hemorrhage, cardiac perfusion eventually diminishes, and multiple organ failure soon
follows.
Stages of Shock
a. Initial Stage
During this stage, the state of hypoperfusion causes hypoxia. Due to the lack of
oxygen, the cells perform lactic acid fermentation. Since oxygen, the terminal electron

acceptor in the electron transport chain, is not abundant, this slows down entry of
pyruvate into the Krebs cycle, resulting in its accumulation. Accumulating pyruvate is
converted to lactate by lactate dehydrogenase and hence lactate accumulates (causing
lactic acidosis).
b. Compensatory stage
This stage is characterised by the body employing physiological mechanisms,
including neural, hormonal and bio-chemical mechanisms in an attempt to reverse the
condition. As a result of the acidosis, the person will begin to hyperventilate in order
to rid the body of carbon dioxide (CO2). CO2 indirectly acts to acidify the blood and
by removing it the body is attempting to raise the pH of the blood. The baroreceptors
in the arteries detect the resulting hypotension, and cause the release of epinephrine
and norepinephrine. Norepinephrine causes predominately vasoconstriction with a
mild increase in heart rate, whereas epinephrine predominately causes an increase in
heart rate with a small effect on the vascular tone; the combined effect results in an
increase in blood pressure. The reninangiotensin axis is activated, and arginine
vasopressin (Anti-diuretic hormone; ADH) is released to conserve fluid via the
kidneys. These hormones cause the vasoconstriction of the kidneys, gastrointestinal
tract, and other organs to divert blood to the heart, lungs and brain. The lack of blood
to the renal system causes the characteristic low urine production. However the effects
of the reninangiotensin axis take time and are of little importance to the immediate
homeostatic mediation of shock.
c. Progressive stage
Should the cause of the crisis not be successfully treated, the shock will proceed to the
progressive stage and the compensatory mechanisms begin to fail. Due to the
decreased perfusion of the cells, sodium ions build up within while potassium ions
leak out. As anaerobic metabolism continues, increasing the body's metabolic
acidosis, the arteriolar smooth muscle and precapillary sphincters relax such that
blood remains in the capillaries.Due to this, the hydrostatic pressure will increase and,
combined with histamine release, this will lead to leakage of fluid and protein into the
surrounding tissues. As this fluid is lost, the blood concentration and viscosity
increase, causing sludging of the micro-circulation. The prolonged vasoconstriction
will also cause the vital organs to be compromised due to reduced perfusion.If the
bowel becomes sufficiently ischemic, bacteria may enter the blood stream, resulting in
the increased complication of endotoxic shock.
d. Refractory stage

At this stage, the vital organs have failed and the shock can no longer be reversed.
Brain damage and cell death are occurring, and death will occur imminently. One of
the primary reasons that shock is irreversible at this point is that much cellular ATP
has been degraded into adenosine in the absence of oxygen as an electron receptor in
the mitochondrial matrix. Adenosine easily perfuses out of cellular membranes into
extracellular fluid, furthering capillary vasodilation, and then is transformed into uric
acid. Because cells can only produce adenosine at a rate of about 2% of the cell's total
need per hour, even restoring oxygen is futile at this point because there is no
adenosine to phosphorylate into ATP
Expected Management in Trauma and Emergency Unit
Restore intravascular volume to reverse the sequence of events leading to inadequate tissue
perfusion.
Redistribute fluid volume
Correct underlying cause of the fluid loss
Ensure patient airway is open, maintaining breathing and circulation.
Administer oxygen at 3-6litre/min by cannula or mask
Restore the circulating blood volume with rapid and blood replacement as prescribed to
optimize cardiac preload, correct hypotension and maintain tissue perfusion.
A central venous pressure catheter is inserted to serve as a guide for fluid replacement.
Continuous CVP reading give the direction and degree of change from baseline readings. The
catheter is also vehicle for emergency fluid replacement.
Large gauge IV needles or catheter are inserted peripheral veins. Two or more catheters may
be necessary for fluid replacement and reversal of hemodynamic instability.
Withdraw sample for: ABGs, chemistry and typing and crossmatch.
Start IV infusion at a rapid rate: Use Ringers Lactate or Normal saline-volume expanders and
adjuncts to blood component therapy.Start transfusion of blood replacement therapy.
Control hemorrhage and carry out continued/serial hemoglobin and hematocrit evaluation.
Maintain the systolic blood pressure by fluids and blood transfusion.
Insert an indwelling urinary catheter, record urine output every 15-30minutes
Carry out rapid physical assessment to determine the cause of shock.

Maintain ongoing nursing surveillance of the total patient Blood pressure, heart rate and
respiratory rate, skin temperature, color, arterial blood gases, ECG, hematocrit hemoglobin,
coagulation profile, electrolytes, and urinary output-so as to assess patient response to
treatment.
Elevate the feet slightly to improve cerebral circulation and promote return of venous blood
to heart.
Give specific pharmacologic agents as prescribed to improve cardiovascular performance.
Reassure and comfort the patient. Sedation may be necessary to relieve apprehension.
Relive pain by cautious use of analgesics or narcotics
Maintain body temperature.
THE CASE
Patient Name: JL
Age: 47 years
Sex: Female
Chief complaint: Semiconscious with retained placenta
Hx Present Illness
The mother is Para 6+0 now at unknown gestation who had home delivery at 6am on day of
admission, and was brought in emergency room at around 12noon in semiconscious state
with retained placenta, and it was reported that she had bled a lot after delivery.At points was
awake and restless, with tachypnea. Appeared pale +++, with initially BPs un-recordable. Her
baby was rushed to neonatal intensive care unit for prematurity care
Past medical/Surgical History
No hx of drug or food allergies, Reports to have been fully immunized, No hx of child hood
illnesses like Measles, mumps, whooping cough, polio, tuberculosis, kwashiorkor or
marasmus. No hx of adulthood/long term illnesses like hypertension, heart diseases, diabetes,
malaria, cancer. No hx of minor or major surgeries, blood transfusion. No hx of serious
accident involvement. OB/GYN history: Para 6 now with 6living children now, no hx of
heavy or painful menstruation, no hx of complication with previous pregnancies, no hx of
abortion.
Family history
She is the 4th born in the family; she has 4 brothers and 3 sisters. No history of any family
members with long term illnesses like, Diabetes, Hypertension, Cancer, Tuberculosis. No
history of any member on long term medication

Social History
She is married, and is a housewife. Went to school up to standard 8. They live in a semipermanent house and sleep under a mosquito net. She does not smoke cigarette or take
alcohol. She is a Christian.
Physical Examination: 29/05/2016 at 12:10pm
GC: In semiconscious state with episodic awakeness accompanied with restlessness and
irritability. Vitals Temp 35.1oC , Pulse 147, Resp 38, BP unrecordable initially then 63/40,
Oxygen sats 57% room air.
CNS:GCS of 13/15, semiconscious, pupils equal and reactive to light with at approx3mm
dilated.
CVS: Initially BPs unrecordable. After bolus 2litre RL, 71/41 then repeat 63/40. With weak
thready pulse of 148beats per minute. S1,S2 head without murmur,also no visible neck vein
distension,capillary refill very slow return. Oxygen saturation 57% room air. With 2 IV
cannula attached to both upper arms peripheral veins.
RESP:Tachypnea 38/min, with deep shallow respiration. Oxygen Saturation of 57% room air,
with labored breathing and no chest in-drawing or retractions. On auscultation, no crackles,
rales or other abnormal breath sounds. Was put on oxygen via Face mask at 8litres/min.
INTEGUMENTARY: Dry lips and skin with poor skin return after skin pinch.
GIT:Dry lips and mucous membranes orally, She asks for water/feels thirsty. Non distended
abdomen with no scars, soft on palpation with positive bowel sounds auscultated in all four
quadrants.
REPRODUCTIVE SYSTEM: Uterus: Was boggy, not well involuted. Had placenta and
membranes retained with hanging cord vaginally.
GUT: Indwelling foley catheter inserted with urine output less than 300ml collected. With
Pale vaginal wall and no active bleeding tears and laceration noted.
MUSC:Equal extremities with unequal powers on all extremities, poor tone.
MISC: Extremities: With palmar pallor and poor capillary nailbed refill. Cold extremities.
IMPRESSION: Typical of hemorrhagic shock-Compensatory stage.

What was done initial contact at Emergency Room


2 IV lines inserted peripheral veins, rapid infusion of 2L of Ringers Lactate
Placenta manually removed-bimanual method (which appeared rugged but complete) and
clots expelled, (approximately 400ml on couch)

Given oxytocin 30IU IM(1st 10IM then repeat 20 IM since IV access was hard to find)
Prostaglandin/Cytotec 800mcg per rectal inserted.
Urinary Foley catheter inserted and connected to urine bag- draining to gravity, with minimal
urine output, approximately 300ml emptied.
Blood Sample collected for Full hemogram/Complete Blood Count and typing and
crosshatching 2 units stat.
After resuscitation and Stabilization, wastransfered to Critical Care Unit for cardiac
monitoring and further management.

LABORATORY INVESTIGATIONS
Parameter
Creatinine (blood)

Normal range
53-97

Msr. Unit
Umol/l

29/05/2016 at 12:40pm
69

Complete Blood Count


WBC
RBC
Hgb
Hct
Platelets
MCV
MCH
MCHC
RDW
Segs
Lymphs
OTHER
BLOOD GROUP

4-11
4.2-5.4
12.0-16.0
36-48
150-500
80-96
27-31
32-36
10-16
40-75
20-50

K/mm3
mil/mm3
g/dL
%
K/mm3
um3
Pg
%
%
%
%
%

6.5
1.91
5.8
15.8
145
82.7
30.4
36.0
15.4
74.4
21.6
9.0
A POSITIVE

PROBLEM LIST
Unrecordable BPs then after bolus 2litres Ringers lactate: Hypotensive 63/40mmHg
Oxygen saturation 57% room air
Altered Mental Status: Confused, restless, irritable and anxious/apprehensive
Dehydration-Dry lips and mucous membranes orally, She asks for water/feels thirsty
Dry lips, and skin with poor return after skin pinch(poor turgor)

Cold extremities
Thready weak pulse/Tachycardia
Urine output of 270ml in the last 8hours
Poor capillary nailbed refill.
Low Hemoglobin of 5.8g/dl, Low RBCs 1.91ml/mm3, low Hct 15.8%.
Low platelets count 145 K/mm3
Blood loss at emergency area approx. 400ml

MEDICATIONS
Dizepam 5mg IV stat
Pethidine 50mg IM stat
Ampicillin 2g IV stat then 1g QID for 48hours
Drug index
DRUG

CLASSIFICA
TION

MODE OF
ACTION

INDICA
TION

Diazepam

Antianxiety

Potentiates
Anxiety
action of
GABA,
especially in
the limbic
system,
reticular
formation ,
enhances
presympathet
ic inhibition

Pethidine

Opioid
analgesic

Depresses
pain
impulses
transmission
at the spinal
cord level by
interacting
with opiod

Moderate
to severe
pain

CONTRA
INDICATI
ON
Hypersens
itivity to
benzodiaz
epines,
glaucoma,
respiratory
depression
, sleep
apnea and
renal
hepatic
disease
Hypersens
itivity

ADVERSE
EFFECTS

NURSING
IMPLICATION

Dizziness,
drowsiness,
orthostatic
hypotension,
blurred vision,
constipation

Assess degree of
Monitor Blood pr
for orthostatic
hypotension
Assess mental sta

Confusion,
sedation,
constipation,
bradycardia,
respiratory
depression

Assess pain, mon


hypersensitivity
Monitor CNS cha
Assess
repiratorydysfuct

Ampicillin

Antibiotic

receptors
Acts
inhibiting
cell wall
synthesis of
susceptible
microorganis
m and thus
killing the
bacteria

Prophyla
xis for
infection

Hypersens
itivity to
penicillins
.

Nausea and
vomiting.
Headache,
Diarrhea.
Chills.

Monitor CBC to
infection process
progression.
Assess for signs o
hypersensitivity.

NURSING DIAGNOSIS
1. Altered tissue perfusion related to decreased circulating blood volume, hypotension
decreased cardiac output as evidenced by Confusion, Hypotensive 63/40mmHg,
Oxygen saturation 57% room air, Cold extremities, thready weak pulse/Tachycardia,
Urine output of 270ml in the last 8hours and poor capillary nailbed refill, Low
Hemoglobin of 5.8g/dl, Low RBCs 1.91ml/mm3, low Hct 15.8%.
2. Impaired gaseous exchange related to reduced oxygen carrying capacity of blood due
to blood as evidenced by Oxygen saturation 57% room air, Cold extremities, thready
weak pulse/Tachycardia, Tachypnea
3. Anxiety related to situational crisis as evidenced by apprehensiveness and restlessness
4. Fluid volume deficit related to decrease intravascular circulation as evidenced by dry
lips and skin, poor skin return on skin pinch(poor turgor) and feeling thirsty,
decreased urine output.
5. Altered urinary elimination(oliguria) related to decreased renal perfusion/decreased
cardiac output as evidenced by urine output of 270ml in the last 8 hours.
6. Risk for Infection related to retained placenta and profuse vaginal bleeding.

CAREPLAN
Assessme Nursing Diagnosis

Expected

nt Data

Outcome

Nursing interventions

Rationale

Evalua s
tion

i
g
n

Confusio
n,
Hypotens
ive
63/40mm

Altered tissue

Patient

perfusion related to

will have

decreased circulating

adequate Continuously monitor

blood volume,

Monitor Vitals signs every To evaluate the patients


15minutes especially BP.

Goal

response to therapy

met,

and to detect

indicat

Hg,
Oxygen
saturation
57%
room air,
Cold
extremiti
es,
thready
weak
pulse/Tac
hycardia,
Urine
output of
270ml in
the last
8hours
and poor
capillary
nailbed
refill,
Low
Hemoglo
bin of
5.8g/dl,
Low
RBCs
1.91ml/m
m3, low
Hct
15.8%.

hypotension

tissue

decreased cardiac

perfusion Monitor hourly urine


in 30
output.
minutes Measure blood loss if

output as evidenced
by Confusion,
Hypotensive

ECG.

possible.

63/40mmHg, Oxygen

Assess level of

saturation 57% room

consciousness,

air, Cold extremities,

mentation, skin

thready weak
pulse/Tachycardia,

temperature, and

Urine output of

peripheral pulses.

270ml in the last

Administer oxygen via

8hours and poor

face mask.
Administer IV fluids

capillary nail-bed

Ringers lactate 3litres.


Transfuse 2 units of blood

refill, Low
Hemoglobin of

cardiopulmonary
deterioration.
To detect life-

ed by
bp
80/50,

threatening

oxyge

dysrythmias of HR >

n sat

140 beats/min, which

92%,

can adversely affect

Patient

Stroke Volume.
To evaluate renal

awake

perfusion.
To ascertain amount of

alert.

and

blood for transfusion.


To evaluate tissue

Pulse

perfusion.
To increase oxygen

in

122/m

carrying capacity of

blood.
stat when ready.
To increase the
Monitor blood gas levels
circulating volume and
and pH
thus enhance

5.8g/dl, Low RBCs


1.91ml/mm3, low
Hct 15.8%.

perfusion.
To enhance oxygen
carrying capacity of
blood and replace lost
blood, so as enhance
perfusion.
changes in blood gases
and pH levels are a
sign of tissue hypoxia

Oxygen

Impaired gaseous

saturation exchange related to


reduced oxygen
57%
room air,

carrying capacity of

Cold

blood due to blood as

extremiti

evidenced by Oxygen
saturation 57% room

Patient
will have

Monitor Vitals signs every To evaluate the patients


15minutes especially BP.

adequate Continuously monitor


gaseous
ECG.
exchange Assess level of
in 30

consciousness,

Patient g

response to therapy

has

and to detect

oxyge

cardiopulmonary

deterioration.
To detect life-

saturat
ion of

es,

air, Cold extremities,

thready

thready weak

weak

pulse/Tachycardia,

pulse/Tac

Tachypnea

minutes

mentation, skin

threatening

95%

temperature, and

dysrhythmias of HR >

via

peripheral pulses.

140 beats/min, which

facem

can adversely affect

ask

Administer oxygen via

hycardia,

Stroke Volume.
face mask at 8litre/min.
To evaluate tissue
Administer IV fluids
perfusion.
Ringers lactate 3litres.
To increase oxygen
Transfuse 2 units of blood
carrying capacity of
stat when ready.
blood.
Position the patient in a
To increase the
semi fowlers position
circulating volume and

Tachypne
a of 38

and
reduce
d
labore
d
breathi
ng.

thus enhance

Resp

perfusion.
To enhance oxygen

24/mi
n

carrying capacity of
blood and replace lost
blood, so as enhance
perfusion.
To reduce efforts in
breathing and thus
reduce oxygen
demand.
Apprehen Anxiety related to

Patient

siveness

situational crisis

will be

and

(changes of

calm and

restlessne circumstances and

less

ss

anxious

fears related to death)


as evidenced by
apprehensiveness and
restlessness.

Encourage the patient and So as to be able to know


family members to
verbalize concerns.
Reassure the patient at
any time.
Administer Diazepam
5mg IV/IM as ordered
by doctor.
Encourage family
members to be around
and encourage.
Be available for the

her concerns and


reassure appropriately.
To enhance patient
calmness and

Patient g
appear
s calm
and
less

cooperation.
appreh
Valium is an antianxiety,
ensive.
will calm the patient
and also sedate.
So that the patient does
not feel left out or
abandoned and also

patient at bedside(Treat
the patient calm,
empathetic and
supportive attitude)
Assess the client's
psychological
response.to the postchildbirth bleeding.
Assess the client's

family members offer


reassurance.
So as to help patient and
meet her immediate
needs.
Perceptions of client
influence the intensity
of anxiety.
Changes in vital signs

physiological responses

lead to changes in the

(tachycardia, tachypnea,

physiological

responses.
shaking).
Provide information about Accurate information
can reduce the anxiety
care and treatment.
and fear of the
unknown.
Dry lips

Fluid volume deficit

Prevent

and skin,

related to decrease

dysfunctio

poor skin

intravascular

nal

return on

circulation as

bleeding

skin

evidenced by dry lips

and

pinch(po

and skin, poor skin

improve

or turgor)

return on skin pinch

fluid

Feeling

(poor turgor) and

volume.

thirsty,

feeling thirsty.

indicated

Monitor intake and output So as to determine


strictly
Assess for dehydration
and document findings
appropriately.
Monitor Vitals signs every

BP
64/30,
Pulse 147

Pulse

cardiopulmonary

mentation, skin
temperature, and
peripheral pulses.
Administer IV fluids

impro

during fluid

emergency room.

increased Monitor hourly urine


intravascu
output.
lar
Assess level of
circulation
consciousness,

100/65
ved,

and to detect

urine

BP

evaluate changes

ECG while in

by

output.

required.
Base line data and to

resuscitation.
15minutes especially BP. To evaluate the patients
Continuously monitor
response to therapy

decreased decreased urine


output.

amount of fluids

Patient g

deterioration.
To detect lifethreatening
dysrhythmias of HR >
140 beats/min, which
can adversely affect
Stroke Volume.
To evaluate renal

112,
Impro
ved
skin
turgor.

Ringers lactate 3litres.


perfusion.
Transfuse 2 units of blood To evaluate tissue
stat when ready.
Do check for electrolyte
in lab.
Advise patients to sleep
with feet higher, while
the body remained
supine

perfusion.
To increase the
circulating volume and
thus enhance
perfusion.
To enhance oxygen
carrying capacity of
blood and replace lost
blood, so as enhance
perfusion.
So as to ascertain
electrolytes imbalance
thus appropriate
measures can be taken.
With feet higher will
increase the venous
return, and allowing
the blood to the brain
and other organs.

Urine

Altered urinary

Patient

output of

elimination(oliguria)

will have

270ml in

related to decreased

improved

the last 8

renal

renal

hours.

perfusion/decreased

perfusion

cardiac output as

in the next

perfusion and

perfusi

evidenced by urine

2hours.

electrolytes imbalance

on

output of 270ml in

thus appropriate

eviden

the last 8 hours.

measures can be taken. ced by

Insert folley catheter and For monitoring strictly


allow draining to
gravity.
Monitor blood creatinine
and electrolytes.

Patient g

input and output and

with

to rule out renal

impro

perfusion.
So as to rule out renal

ved
renal

urine
out put
of
400ml
after

interve
ntions
Risk for Infection

The

related to retained

patient

placenta and profuse

will not

vaginal bleeding.

develop
infection.

Monitor vital signs and


note changes in

Changes in vital signs

Not an

(temperature) is

infecti

temperature.
indicative of infection.
Note the signs of fatigue, The signs are an

on
(lochia

chills, anorexia, uterine

indication of the

is no

contractions were

occurrence of

smell ,

flabby, and pelvic pain.


bacteremia.
Administer Ampicillin 2g For prophylaxis and
IV stat and then 1g QID

prevent infection.
for 48hours as ordered. Infection prevention
Institute infection
measures helps protect
prevention measures as
per hospital protocol.
Use of aseptic techniques

the patient, nurse and


other health care

workers.
in indicated procedures To prevent introduction
like insertion of

indwelling catheter.
Monitor or order full
hemogram(CBC)

and
vital
signs
within
norma
l
limits)

of infection.
Elevated WBCs are
indicator for possible
infection.

especially WBCs.

Signs and symptoms of Shock:

CONCEPT MAP
SHO
Definition: state of
cellular and tissue
hypoxia due to
reduced oxygen
delivery and/or
increased oxygen
consumption or

Types of Shock:
a.Hypovolemic shock
b.Cardiogenic shock
c.Distributive shock
d.Obstructive shock

A rapid, weak, thready pulse due


to decreased blood flow
combined with tachycardia
Cool, clammy skin due
to vasoconstriction and
stimulation of vasoconstriction
Rapid and shallow breathing due
to sympathetic nervous system
stimulation and acidosis
Hypothermia due to decreased
perfusion and evaporation of
sweat
Thirst and dry mouth, due to
fluid depletion
Cold, and mottled skin (Livedo
reticularis), especially
extremities, due to insufficient

Stages of Shock:
a. Initial stage
b. Compensatory
stage
c. Progressive stage
d. Refractive stage
Diagnostic tools
Labs: CBC, Cr, K, Na,
ABGs
History and P.E

Altered tissue perfusion


related to decreased
circulating blood volume,
hypotension decreased
cardiac output as
evidenced by Confusion,
Hypotensive, Oxygen
saturation 57% room air,
Cold extremities, thready
weak pulse/Tachycardia,
Urine output of 270ml in
the last 8hours and poor
capillary nailbed refill, Low

COLLABORATIVE MANAGEMENT IN EMERGENCY ROOM


Ensure patient airway is open, maintaining breathing and circulation.
Restore intravascular volume to reverse the sequence of events
leading to inadequate tissue perfusion.
Redistribute fluid volume
Correct underlying cause of the fluid loss
NURSING
Administer oxygen at 3-6litre/min by cannula or mask
Restore the circulating blood volume with rapid and blood replacement
DIAGNOSIS
as prescribed to optimize cardiac preload, correct hypotension and
maintain tissue perfusion.
Impaired gaseous
Large gauge IV needles or catheter are inserted peripheral veins. Two
exchange related to
or more catheters may be necessary for fluid replacement and
reduced oxygen carrying
reversal of hemodynamic instability.
Withdraw sample for: ABGs, chemistry and typing and crossmatch.
capacity of blood due to
Start IV infusion at a rapid rate: Use Ringers Lactate or Normal salineblood as evidenced by
volume expanders and adjuncts to blood component therapy. Start
Oxygen saturation 57%
transfusion of blood replacement therapy.
room air, Cold
Control hemorrhage and carry out continued/serial hemoglobin and
extremities, thready
hematocrit evaluation.
weak pulse/Tachycardia,
Maintain the systolic blood pressure by fluids and blood transfusion.
Insert an indwelling urinary catheter, record urine output every 1530minutes
Anxiety related to
Carry out rapid physical assessment to determine the cause of shock.
situational crisis as
Maintain ongoing nursing surveillance of the total patient Blood
evidenced by
pressure, heart rate and respiratory rate, skin temperature, color,
apprehensiveness and
arterial blood gases, ECG, hematocrit hemoglobin, coagulation
restlessness
profile, electrolytes, and urinary output-so as to assess patient
response to treatment.
Fluid volume deficit
Elevate the feet slightly to improve cerebral circulation and promote
related to decrease
return of venous blood to heart.
REFERENCES
intravascular circulation
Give specific pharmacologic agents as prescribed to improve
as evidenced by dry lips
cardiovascular performance.
Lewis S.M., Heitkemper M.M., Dirksen S.R., (2000). Medical Surgical Nursing; Assessment and
Reassure and comfort the patient. Sedation may be necessary to
and skin, poor skin
th
relieve apprehension.
management of Clinical Problems. 5 Edition. St Louis Missouri, Mosby.
return on skin pinch
Relive pain by cautious use of analgesics or narcotics
(poor turgor) and feeling

Maintain body
temperature.
thirsty, decreased urine
Gordon
, M.(2000) Manual of Nursing diagnosis: 1995-1996. St Louis Missouri, Mosby.

George Krucik,(No date). What causes shock.Retrieved from


http://www.healthline.com/symptom/shock

Paul K.,(n.d) Hypovolemic shock. Retrieved from


http://emedicine.medscape.com/article/760145-overview#a6
Shock(Circulatory). (2016, May 28) Retrieved from
https://en.wikipedia.org/wiki/Shock_(circulatory)
Brunner &Suddarths, (2010). Textbook of Medical-Surgical Nursing. 10th edition. St Louis
Missouri, Mosby.

Jones & Bartlett Learning, LLC (2011) Nurses Drug Handbook Tenth Edition

Potrebbero piacerti anche