Life-threatening conditions

1. EVELYN M. BALANQUIT, MAN
Clinical Instructor

2. Acute Renal failure:
 Is the sudden interruption of kidney function from
obstruction, reduced circulation, renal
parenchymatous disease
 a sudden loss of kidney function caused by failure of
renal circulation or damage to the tubules or
glomeruli.
 Usually irreversible with treatment, but can progress
to end- stage renal disease, uremic syndrome or death.

3. Etiologic factors
 Prerenal - caused by decrease blood flow to kidneys
like severe dehydration, diuretic therapy, circulatory
collapse, hypovolemia or shock; readily reversible
when recognized and treated
 Intrarenal – caused by disease process, ischemia, or
toxic conditions such as acute glomerulonephritis,
vascular disorders, toxic agents, or severe infection
 Post renal – caused by any condition that obstructs
urine flow such as benign prostatic hyperplasia, renal
or urinary tract calculi, or tumors.

4. Pathophysiology
 Acute renal failure is classified as prerenal, intrarenal
or post renal. All conditions that lead to prerenal
failure impair blood flow to the kidneys (renal
perfusion), resulting in a decreased glomerular
filtration rate and increased tubular desorption of
sodium and water. Intrarenal failure results from
damage to the kidneys. Post renal failure results from
obstructed urine flow

5. Clinical Manifestations
*A change in blood pressure and volume signals pre
renal failure, the patient may have the following:
 -Oliguria
 -Tachycardia
 -Hypotension
 -Dry mucous membranes
 -Flat jugular veins
 -Lethargy progressing to coma
 -Decreased cardiac output
 -Cool, clammy skin in patient with heart failure

6. Clinical Manifestations
*As renal failure progresses, the patient may manifest
the following signs and symptom:
 - uremia
 - confusion
 - GI complaints
 - fluid in the lungs
 - infection

7. Diagnostics
 Blood studies reveal elevated BUN, serum creatinine, and
potassium levels and decreased blood pH, bicarbonate,
Hct, and Hgb levels
 Urine studies show casts, cellular debris, decreased specific
gravity and, in glomerular diseases, proteinuria and urine
osmolality close to serum osmolality
 Creatinine clearance testing is used to measure the GFR
and estimate the number of remaining functioning
nephrons
 Electrocardiogram (ECG) shows tall, peaked T waves,
widening QRS complex, and disappearing P waves if
increased potassium is present

8. Diagnostics
*Other studies used to determine the cause of renal
failure:
 kidney ultrasonography
 plain films of the abdomen
 KUB radiography
 excretory urography
 renal scan
 retrograde pyelography
 computed tomography scan and
 nephrotomography

9. Treatment:
Goal: - establish an effective renal function
- maintain the constancy of the internal
environment despite transient renal failure.
1. Supportive measures
2. Manage hyperkalemia
3. Hemodialysis or peritoneal dialysis

10. Nursing Diagnoses
 Excess Fluid Volume
 Imbalanced Nutrition: Less than Body Requirements
 Deficient Knowledge
 Risk for Infection

11. Nursing Care:
 Monitor intake and output
 Monitor the vital signs
 Weigh daily and observe for edema
 Avoid medications with potassium
 Observe for oliguria followed by polyuria
 Monitoring of complications of electrolyte
imbalances, such as acidosis and
hyperkalemia

12. Nursing Care:
 Encourage prescribed diet: moderate protein
restriction, high in carbohydrates, restricted
potassium
 Assess hemodynamic results
 Watch for and report signs and symptoms of
pericarditis
 Allow client to verbalize concerns regarding disorder
 Once diuresis phase begins, evaluate slow return of
BUN, creatinine, phosphorus, and potassium to
normal

13. Pharmacologic Therapy:
 Kayexalate ( cation exchange resins) to reduce serum
potassium levels and sodium bicarbonate to treat
acidosis
 Use volume expanders are prescribed to restore renal
perfusion in hypotensive clients and Dopamine IV to
increase renal blood flow
 Loop diuretics to reduce toxic concentration in
nephrons and establish urine flow
 ACE inhibitors to control hypertension
 Antacids or H2 receptor antagonists to prevent gastric
ulcers
 *Avoid nephrotoxic drugs

14. Client Education
 Dietary and fluid restrictions, including those that
may be continued after discharge
 Signs of complications such as fluid volume excess,
CHF, and hyperkalemia
 Monitor weight, blood pressure, pulse, and urine
output
 Avoid nephrotoxic drugs and substances: NSAIDs,
some antibiotics, radiologic contrast media, and heavy
metals; consult care provider prior to taking any OTC
drugs
 Recovery of renal function requires up to 1 year; during
this period, nephrons are vulnerable to damage from
nephrotoxins

15. Stroke (CVA)
 Is a sudden interruption of circulation in one or more
of the blood vessels supplying the brain
 Sudden loss of function resulting from disruption of
blood supply to a part of the brain.
 Brain tissue fails to receive adequate oxygenation,
resulting in serious tissue damage or necrosis.

16. CAUSES
 Thrombosis of the cerebral arteries supplying the
brain or of the intracranial vessels occluding blood
flow
 Embolism from a thrombus outside thebrain, such as
in the heart, aorta, or common carotid artery
 Hemorrhage from an intracranial artery or vein, such
as from hypertension, ruptured aneurysm, AVM,
trauma, hemorrhagic disorder, or septic embolism

17. Pathophysiology
 The underlying event leading to stroke is oxygen and
nutrient deprivation; if the arteries become blocked,
auto regulatory mechanisms maintain cerebral
circulation until collateral circulation develops to
deliver blood to the affected area; if the compensatory
mechanisms become overworked or cerebral blood
flow remains impaired for more than a few minutes,
oxygen deprivation leads to infarction of brain tissue

18. Risk factors
 Hypertension
 Family history of stroke
 History of TIA
 Cardiac disease, including arrhythmias, coronary
artery disease, acute myocardial infarction, dilated
myopathy, and alular disease
 Diabetes mellitus
 Familial hyperlipidemia
 Cigarette smoking
 Increased alcohol intake
 Obesity, sedentary lifestyle
 Use of hormonal contraceptives

19. Clinical manifestations:
 Sudden onset of:
- headache with no known cause
- numbness or weakness of the face, arm or leg
especially on one side of the body (generally on the same
side as the hemiparesis)
- confusion, trouble speaking or understanding
- trouble seeing or walking
- dizziness,
- loss of coordination
 Motor loss:
- hemiplegia
- hemiparesis on the affected side (may be more severe in
the face and arm than in leg)

20. Clinical manifestations:
 Communication loss:
- dysarthria
- dysphasia
- aphasia
- apraxia
 Perceptual disturbances:
- hemianopsia
 Sensory loss:
- agnosias
- blurred or indistinct vision, double vision, or vision loss in one
eye (usually described as a curtain coming down or gray-out of
vision)
 Cognitive impairment & psychological effects
-Mental status changes or loss of consciousness (particularly if
associated with one of the above symptoms)
*A stroke in the left hemisphere produces symptoms on the right side of
the body; in the right hemisphere, symptoms on the left side.

21. Diagnostic Examinations
 MRI or is used to identify areas of ischemia, infarction and
cerebral swelling
 CT scan discloses structural abnormalities, edema, and
lesions, such as no hemorrhagic infarction and aneurysms
 Cerebral Angiography shows details of disruption or
displacement of the cerebral circulation by occlusion or
hemorrhage
 DSA is used to evaluate patency of thecerebral vessels and
shows evidence of occlusion of the cerebral vessels, a lesion
or vascular abnormalities
 Carotid Duplex scan is a high frequency ultrasound that
shows blood flow through the carotid arteries and reveals
stenosis due to atherosclerotic plaque and blood clot

22. Diagnostic Examinations
 Brain scan shows ischemic areas but may not be
conclusive for up to 2 weeks after stroke
 Tran’s cranial Doppler studies are used to evaluate the
velocity of blood flow through major intracranial
vessels, which can indicate vessel diameter
 Single photon emission CT scanning and PET scan
show areas of altered metabolism surrounding lesions
that aren’t revealed by other diagnostic tests
 EEG is used to identify damaged areas of the brain and
to differentiate seizure activity from stroke

23. Diagnostic Examinations
 Lumbar puncture reveals bloody CSF when stroke is
hemorrhagic
 Ophthalmoscopy reveals visual changes
 Laboratory studies
- CBC, platelet count, and chemistry panel are obtained
before thrombolytic therapy
- A blood glucose test shows whether the patient’s
symptoms are related to hypoglycemia
-Hemoglobin and hematocrit level may be elevated in
severe occlusion
- PTT, PT, fibrinogen level
- electrolytes
- lipid profile, BUN, Creatinine
- urinalysis

24. Nursing Diagnoses
 Ineffective Tissue Perfusion related to decreased
cerebral blood flow
 Risk for Prolonged Bleeding related to use of
thrombolytic agents
 Increased Risk for Aspiration related to depressed gag
reflex, Impaired swallowing
 Impaired Physical Mobility related to loss of muscle
tone

25. Nursing Care:
 Maintain a patent airway and oxygenation
 Check vital signs and neurologic status
 Watch signs & symptoms of pulmonary emboli
- chest pain
- shortness of breath
- fever and change of sensorium
-tachycardia
 Monitor ABG levels
 Maintain fluid and electrolyte balance

26. Nursing Care:
 Encourage active range of motion on unaffected side
and passive range of motion on the affected side
 Turn client every 2 hours
 Monitor lower extremities for thrombophlebitis
 Encourage use of unaffected arm for ADLs
 Teach client to put clothing on affected side first

27. Nursing Care:
 Manage GI problems
 Clean and irrigate the patients mouth and dentures to
remove food particles
 Help patient exercise
 Collaborate with occupational and physical therapists
 Administer medication as ordered
 Ensure adequate nutrition
 Resume diet orally only after successfully completing
swallowing evaluation

28. Nursing Care:
 Maintain communication with the patient.
 Try alternate methods of communication with aphasia
patients
 Accept client’s frustration and anger as normal to loss
of function
 Teach client with homonymous hemianopia to
overcome the deficit by turning the head side to side to
be able to fully scan the visual field

29. Pharmacologic Therapy
 Aspirin or ticlopidine (Ticlid)as an antiplatelet agent to
prevent recurrent stroke
 Benzodiazipines (diazepam) to treat patients with seizure
activity
 Anticonvulsants to treat seizures or to prevent them after
the patient’s condition has stabilized
 Analgesics to relieve the headaches that may follow
hemorrhagic stroke

30. Pharmacologic Therapy
 Thrombolytics (ateplase) for emergency treatment of
ischemic stroke
 Stool softeners to avoid straining, which increase ICP
 Hyperosmolar solutions (Mannitol) or diuretics are
given to clients with cerebral edema
 Antihypertensives and antiarrhythmics to treat
patients with risk factors for recurrent stroke
 Corticosteroids (dexamethasone) to minimize
associated cerebral edema

31. Surgical Intervention
• Craniotomy to remove hematoma
• Carotid endarterectomy to remove atherosclerotic
plaques from an arterial wall or extracranial bypass to
circumvent or blocked artery
• Extra cranial bypass to circumvent an artery
that’s blocked by occlusion or stenosis

32. Client Education
 Educate client and family about CVA and CVA
prevention
 Educate client and family about community resources
 Educate client and family about physical care and need
for psychosocial support
 Educate client and family about medication

33. Increased Intracranial Pressure
 prolonged pressure greater than 15 mm Hg o r 180
mm H2O measured in the lateral ventricles
 Etiology
-Cerebral Edema is an increase in volume of brain
tissue due to alterations in capillary permeability,
changes in functional or the structural integrity of
the cell membrane or an increase in the
interstitial fluids
-Hydrocephalus is an increase in the volume of
CSF within the ventricular system; it may be no
communicating hydrocephalus where the
drainage from the ventricular system is impaired

34. Pathophysiology
 Blood flow exerts pressure against a weak arterial wall,
stretching it like an overblown balloon and making it
to rupture; rupture is followed by a subarachnoid
hemorrhage, in which blood spills into space normally
occupied by CSF. Sometimes, blood spills into brain
tissue, where a clot can cause potentially fatal
increased ICP and brain tissue.

35. Clinical manifestations
a. Early signs:
A decrease or change in LOC
1. Confusion to restlessness
2. Irritability & agitation
3. Lethargy to stupor
4. Disoriented to 3 spheres (time, place & person)
5. Doesn’t respond to question

36. Clinical manifestations
 b. Late signs:
1. Change in the vital signs:
 Hypertension (SBP rises while DBP remains the same)
140/80 mm Hg
Widened pulse pressure 60 mmHg
(normal adult BP 120/80; pulse pressure 40 mmHg)
 Bradycardia
 Bradypnea (Cheyne Stokes respiration) slow, irregular
respiration/hyperventilation with periods of apnea
 Hyperthermia
CUSHING’S TRIAD: hypertension, bradycardia,
bradypnea

37. Clinical manifestations
2. Projectile vomiting
3. Headache
4. Possible seizure
There is a ICP monitoring device usually connected
into the lateral ventricles of subarachnoid space.

38. Diagnostics
 -Skull radiography
 -CT scan
 -MRI
 * Lumbar puncture is not performed because of brain
herniation caused by sudden release of pressure
 Laboratory tests are performed to augment and
monitor treatment approaches;
 serum osmolality monitors hydration status and ABGs
measure pH, oxygen and carbon dioxide

39. Nursing Diagnoses
 Ineffective Cerebral Tissue Perfusion related to
Increased ICP
 Risk for Infection
 Impaired Physical Mobility
 Risk for Ineffective Airway Clearance

40. Nursing Management
 Assess neurological status every 1 to 2 hours and report
any deterioration; include LOC, behavior,
motor/sensory function, pupil size and response, vital
signs with temperature
 Maintain airway; elevate head of 30 degree or keep flat
as prescribed; maintain head and neck in neutral
position to promote venous drainage
 Assess for bladder distention and bowel constipation;
assist client when necessary to prevent Valsalva
maneuver

41. Nursing Management
 Plan nursing care so it is not clustered because
prolonged activity may increase ICP
 provide quiet environment and limit noxious stimuli
 limit stimulants such as radio, TV and newspaper;
avoid ingesting stimulants such as coffee, tea, cola
drinks and cigarette smoke
 Maintain fluid restriction as prescribed
 Keep dressings over catheter dry and change dressings
as prescribed; monitor insertion site for CSF leakage or
infection; monitor clients for signs and symptoms of
infection; use aseptic technique when in contact with
ICP monitor

42. Pharmacologic therapy
 Osmotic diuretics such as Mannitol and loop diuretics
such as Furosemide (Lasix) are mainstays used to
decrease ICP
 Corticosteroids are effective in decreasing ICP
especially with tumors

43. Surgical Intervention
 A drainage catheter, inserted via ventriculostomy into
lateral ventricle, can be done to monitor ICP and to
drain CSF to maintain normal pressure; if used the
system is calibrated with transducer is leveled 1 inch
above the ear; sterile is of utmost importance

44. Client Education
 Teach the client at risk for increased ICP to avoid
coughing, blowing the nose, straining for bowel
movements, pushing against the bed side rails, or
performing isometric exercises
 Advice the client to maintain neutral head and neck
alignment
 Encourage the family to maintain quiet environment
and minimize stimuli
 Educate the family that upsetting the client may
increase ICP