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HEPATIC COMA/ENCEPHALOPATHY
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Wh at is Sh ock ?
A. HY PO VO LEMI C SHO CK
External:FluidLoss
Internal:FluidShift
trauma a. hemorrhage
surgery b. burns
vomiting c. ascite
diarrhea d. peritonitis
diuresis e. dehydration
diabetes insipidus
Med ica l M an agemen t
GOALS:
restore intravascular volume
redistribute fluid volume
correct the underlying cause
Desmopressin
Insulin
Anti-emetic
Anti-diarreal
Nu rs in g M anagemen t
Closely monitor px at risk for fluid deficits(younger than 1y/o or
65 years of age)
Reduce fear and anxiety about the need for oxygen mask by
giving px explanations and frequent reasurance
Ca rdiog en ic Sh oc k
Ca rdiog en ic Sh oc k
Angina pain
Hemodynamic instability
Classic sign like low blood pressure, rapid and weak pulse.
Ø supplemental oxygen
Ø controlling chest pain
Ø selected fluids support
Ø vasoactive medications
Ø controlling heart rate
Ø mechanical cardiac support
e.g intra-aortic balloon counterpulsation, ventricular
assist sysytem.
Dobutamine
Dopamine
Anti-arrythemic meds
Nitroglycerine
Vasoactive meds
Nu rs in g M anagemen t
Immunosuppression
Extremes of age ( younger than 1y/l and older
than 65y/o)
Alcoholism
Extensive trauma of burns
Malnutrition
Diabetes
Malignancy
Chronic illness
Invasive procedures
Pathop hysiolog y
Reduce px temp. when ordered for temp above 104.8F (40.8C) monitor
closely for shivering
Monitor and report blood levels (antibiotics, BUN, creatinine, WBC ) and
hemodynamic status, fluid IO and nutritional status.
Monitor daily wts. And serum albumin levels to determine daily protein
requirements
NE UR OLOG IC SHO CK / S PI NAL
SHOC K
Spinal anesthesia
Depressant meds
Hypoglycemia
Med ica l M an agemen t
Feet elevation
Passive ROM
An aphylactic S hock
An aphylactic S hock
Drug sensitivity
Transfusion reaction
Bee sting allergy
Latex sensitivity
Med ica l M an agemen t
Patient education
Sta ges of Sh ock
Myocardial depression
D. Renal effects
Ø MAP<80mmHg
Ø Acute renal failure
E. Hepatic effects
Ø Decreased blood flow
Ø Less ability to perform hepatic functions
F. gastrointestinal effects
Ø Decreased blood flow
Ø PUD
Ø Bloody diarrhea
Ø Sepsis
Med ica l M an agemen t
B. La te sta ges
Ø Shallow respiration, decreased BP, increased PR, hypothermia
Ø Oliguria, Anuria
Ø Hyperkalemia
Ø Metabolic acidosis
Ø Edema
Ø Cool clammy skin- hypovolemic, cardiogenic and septic shock
Ø Lethargy, dilated pupils
Ø Decreased bowel sounds
Ø Cyanosis
Ø DIC
Interv en tion s
A. Promoti ng flu id s balance
Ø Blood transfusions
Ø IV fluids
F. Promotin g sa fety
Ø Soft restraints as needed
Ø Practice strict asepsis
Ø Prevent complications of immobility
Ø Protect from chills
Drug Th er apy
Vas oco nst ri ct ors:
Norepi ne phr ine / epi nep hri ne, do pa min e, dobu tam
Vaso dila tors:
Nitr ate s lik e nitr ogly cer ine an d Iso so rb ide
Na+ bicarbonate to reverse acidosis
Antibiotics to control sepsis
Heparin to treat DIC
Steroids to reduce inflammation
H2 antihistamines, Ranitidine, cimetidine
Glucose 50% or glucagons to increased blood sugar
Narcotics for pain
Antidysrrhythamic drugs
End of the slides
Arrh yth mia s
Card ia c Arr hythmia s
As the heart rate increases, the diastolic falling time decreases, result in
reduced cardiac output and subsequent symptoms of syncope and low
blood pressure. If the heart cannot compensate for the decreased
ventricular falling the px may develop acute pulmonary edema
Ma nag eme nt
B. At ri al Fl utt er
Occur in the atrium and creates impulse at an atrial
rate between 250 and 400 time per minute.
Chest pain
Shortness of breath
Low blood pressure.
Ma nag emen t
The shorter time in diastole reduce the time available for coronary
artery perfusion, there by increasing the risk for myocardial ischemia.
Calcium channel blocker and beta blocker are effective in controlling the
ventricular rate in atrial fibrillation
Use Digoxin is recommended to control the ventricular rate those patient with
poor cardiac function
Is an impulse that starts in the AV nodal before the next normal sinus
impulse reaches the AV node Premature junction complex are less common
than PAC’s
The criteria for premature junction complex are the same as for PACs except
for the Pwave and the PR interval. The Pwave may be absent QRS, or may
occur before the QRS but with a PR interval of less than 0.12 second
The wave of impulse originates from an ectopic Focus (Foci) within the
ventricles at rate faster than the next normally occurring beat.
The Clinical sign and symptoms of a heart block vary with the
resulting ventricular rate and the severity of any underlying
disease processes.
Second degree type I heart block occurs when all but one of the
atrial impulse are conducted. Through the AV node into the ventricles.
Each atrial impulse a take longer time for conduction than the one
before, until one impulse is fully blocked.
Ch aract erist ics :
Regularly evaluate the blood pressure, pulse rate and rhythm, rate and
depth of respiration and breath sounds to determine the hemodynamic
effects.
Goal is to maximize the client’s controls and to make the unknown less
threatening.
Leads can be threaded through a major veins into the right ventricles
(endocardial leads) or they can be lightly sutured onto the outside the
heart and brought the chest wall during open heart surgery.
Pa cema ker D es ig n a nd
types
Epicardial wires are always temporary and are removed by
a gentle tug within a few daysafter surgery.
Caus es:
Cerebral arteriosclerosis
Syphilis
Trauma
Hypertension
Thrombosis
Embolism
Hemorrhage
Vasospasm
Ty pes of S trok e
Visual disturbance
Vital sign monitored q 15min for the first 2 hrs,q30 min for the next 6
hrs.
Some clinicians advocate the use of a properly worn sling when the
patients first becomes ambulatory to prevent upper extremity from
dangling without support.
3. M an ag e D ysph agia
ISCHEMIC STROKE
HEMORRHAGIC STROKE
Hemor rh agic St ro ke
Primarily caused by an intracranial or subarachnoid
hemorrhage, bleeding into the brain tissue, the
ventricles, or subarachnoid space.
Bleeding into the brain substance, common in patients with hypertension and
cerebral atherosclerosis that causes rupture of the vessel
Brain tumor and the use of medicines( oral anticoagulants, amphetamines and
illicit drugs such as crack and cocoaine).
Bleeding occur mostly in the cerebral lobes, basal ganglia, thalamus, brain
stem (mostly pons) and cerebellum
Avoid Valsalva maneuver, straining , forceful sneezing, pushing up to bed, acute flexion or
rotation of the head and neck.
No enemas are permitted but stool softener and mild laxative is prescribed.
Observed for the s/sx of deep vein thrombosis such as tenderness, swelling, warmth,
discoloration, positive Homan’s sign report any abnormal findings
Depth of the injury depends on the temperature of the burning agent and the
duration of contact with the agent
The epidermis and upper to uper deeper portion of the dermis are
injured. eg, scald
The wound is painful, appears red, and exudes fluid. Capillary
refill follows tissue blanching.
Hair follicles remain intact.
Deep partial-thickness burns take longer to heal and are more
likely to result in hypertrophic scars.
Secon d D egree Bu rn
Cl assi fica tio ns of Bur n
Ac co rdi ng to D epth o f Ti ssu e
Destr uc tio n
C. Full – Thickness Burn
(third degree burn)
B. Mi dd le zo ne
has a compromised blood supply, inflammation, and
tissue injury.
C. Outer zo ne
the zone of hyperemia which sustains the least
damage.
RU LE O F NI NE
9 18 18 9 PARKLAND FORMULA
Computation of fluids
Most commonly used in burned patient
1
Focus on the major priorities of any trauma patient: ABC, disability, exposure,
and fluid resuscitation.
Note any increased hoarseness, stridor, abnormal respiratory rate, and depth, or
mental changes from hypoxia.
Fluid volume deficit r/t increased capillary permeability and evaporative fluid
loss from burn wound.
Pain r/t tissue and nerve injury and emotional impact of injury.
Provide pain releif, and give antianxiety med if px remain highly anxious and
agitated.
Nu rs in g I nter ven tion
5. Mon ito r an d Ma nagi ng Pote nti al Comp lica ti on s
Ac ute Re spir atory Failu re : assess for increasing dyspnea. Stridor,
changes in respiratory patterns; monitor arterial blood gas (ABGs),
pulse oximetry to detect problematic oxygen saturation and increasing
carbon monoxide; monitor chest x-rays for cerebral hypoxia
Dis tri bu tiv e Shock : monitor for early signs of shock or progressive
edema. Administered fluid resuscitation as ordered in response to
physical findings; continue monitoring fluid status
Ac ute Re nal Fa ilu re : monitor and report abnormal urine output and
quality
Com pa rtme nt Syndr ome : assess nuerovascular status of extremities
hourly; report any extremity pain, loss of peripheral pulse or sensation
Paralyt ic Ileu s: NGT and maintain in low intermittent suction until
bowel sound resume
Cu rli ng’ s Ulce r: assess gastric aspirate for blood and pH; assess
stools for occult blood; administerd antacids and histamine blockers
(eg, ranitidine, (zantac)) as prescribed.
Acu te and In term edi ate P ha se
It b egins 42 to 72 hours aft er t he b urn inju ry. Burn wo und care and
pai n cont ro l are the p riori ties i n thi s st ag e
Assessment
- Focus on hemodynamic changes
- Measure V/S frequently
- Assess peripheral pulses frequently
- Observe electrocardiogram for dysrhythmias resulting from potassium
imbalance
- Assess residual gastric volume and pH in px with NGT
- Note and report blood in gastric fluid or stool.
- Assess wound: size, color, eschar, exudate, abscess formation under the
eschar, epithelial buds, bleeding granulation tissue appearance
- Focus on pain and psychosocial response
- Assess for excessive bleeding adjacent to areas of surgical exploration
and debridement
Dia gnos is
Risk for infection related to loss of skin barrier and impaired immune
response
Impaired physical mobility r/t burn wound edema, pain, and joint
contractures
4. Promot e Sk in Int eg ri ty
Asses wound status
Support px during distressing and painful wound care
Coordinate complex aspects of wound care
Assess and record any changes and progress in wound healing
Assist, instruct, support, and encourage px and family to take part in dressing
changes and wound care.
Document participation and self care abilities in wound care and ambulation
Pr even tio n
For obese patients(especially those with type 2 diabetes): weight loss is the
key to treatment and the major preventive factor for the development of
diabetes
Managemen t
Use of oral hypoglycemic agents if diet and exercise are not successful
in controlling blood glucose levels. Insulin injections may be used in
acute situations
Reduce anxiety
(5) Hyperglycemia, due to decreased use of glucose by the cells and increased
production of glucose by the liver;
(7) Dehydration and electrolyte loss, resulting from polyuria, with a loss of up to
6.5 liters of water and up to 400 to 500 mEq each of sodium, potassium, and
chloride over 24 hours; and
(9) Acidosis, due to an excess breakdown of fatty acids and production of ketone
bodies, which are also acids. Three main causes of DKA are decreased or
missed dose of insulin, illness or infection, and initial manifestation of
undiagnosed or untreated diabetes.
Clin ica l M anifes tatio ns
Polyuria, polydipsia (increased thirst)
Acetone breath
Kaussmauls respiration
Teach the patient about “sick-day rules” which are strategies to help
prevent diabetic complications.
Do not eliminate insulin doses when nausea and vomiting occur
Take usual insulin dose or previously prescribed sick-day doses and attempt to
consume frequent small portions of carbohydrates
Drink fluids every hour to avoid dehydrations
Check blood glucose level every 3-4 hours
End of the slides
Hepatic En ce phalop ath y
CBC – pancytopenia
PTT – prolonged
Monitor serum ammonia level daily; monitor electrolyte status and correct if
abnormal
Hypertension
Chronic glomerulonephritis
Pyelonephritis
Vascular disorder
Infections
Uremia develops
Integu me ntary: ecchymosis, purpura, thin brittle nails, coarse thinning hair, gray-bronze
skin color, dry flaky skin
Ga str oin test in al: ammonia odor of breath, metallic taste, mouth ulceration and
bleeding,N/V, constipation or diarrhea, bleeding in GIT
Musculos kel eta l: muscle craps, loss of muscle strength, renal osteodystrophy, bone
pain, fracture, foot drop
Rep rodu cti ve: amenorrhea, testicular atrophy, infertility, decrease libido
3. An emia
Inadequate erythropoietin production
Producing fatigue, angina and shortness of breath
Antacids
Hyperphosphatemia and hypocalemia are treated with aluminium based antacid
Magnesium based antacid should be avoided to prevent magnesium toxicit
Med ica l M an agemen t
2. Di et ther ap y
Vitamin supplementation
CHON restriction
Potassium restriction
3. Dial ys is
Used to remove fluid and uremic waste products from the body when the kidney cannot
do so.
Used to treat px with edema that does not respond to tx, hepatic coma, hyperkalemiam
hypercalcemiam HPN and uremia
Ty pes of D ia lys is
Med ica l M an agemen t
Meth ods of Thera py Complication includes:
Report the health care provider the s/sx of decreased renal fxn
CAUSES:
• Hypovolemia
• Sudden increased in intravascular pressure in the
lung
• Inadequate liver function
Pathop hysiolog y
Patient hands become cold and moist the nailbeds are cyanotic
Crackles are due to the movement of air through the alveolar fluid
Tachycardia, the pulse oximetry values begins to fall and arterial blood
gads analyzing demonstrates increased hypoxemia
Med ica l man agemen t
Monitor I and O
Massive pulmonary embolism is life threatening and can cause death within
the first 1 to 2 hours after the embolic event.
Symptoms depend on the size of the thrombus and the area of the
pulmonary artery occlusion.
Dyspnea is the most common symptom. Tachypnea is the most frequent sign
Chest pain is common, usually sudden in onset and pleuritic in nature; it can
be substernal and may mimic angina pectoris
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