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Acute Biologic Crisis

CRITICAL CARE NURSING

nurse licensed professional who provides care to meet the


patient s individualized needs in response to potentially
life-threatening conditions in an environment supportive
of
highly technological, collaborative and holistic care.
 The intensive care unit is not merely a
room or series of room filled with
patients attached to interventional
technology; it is the home of an
organization : the intensive care team.
THE INTENSIVE CARE
TEAM
 Doctor
 Nurses
 Therapists
 Nutritionists
 Chaplains and other support staff, builds
an environment for healing or dying.
LEVELS OF ICU CARE
 LEVEL I – PROVIDES MONITORING,
OBSERVATION AND SHORT TERM
VENTILATION.

 LEVEL II – PROVIDES
OBSERVATION, MONITORING &
LONG TERM VENTILATION WITH
RESIDENT DOCTORS.
 LEVEL III – PROVIDES ALL ASPECTS
OF INTENSIVE CARE INCLUDING
INVASIVE HEMODYNAMIC
MONITORING & DIALYSIS.
 Critical care nursing is that specialty
within nursing that deals specifically with
human responses to life-threatening
problems
SEVEN Cs OF CRITICAL
CARE
 Compassion
 Communication
 Consideration (to patients, relatives and
colleagues) and avoidance of Conflict.
 Comfort: prevention of suffering
 Carefulness (avoidance of injury)
 Consistency
 Closure (ethics and withdrawal of care )
CRITICAL CARE NURSE
 A critical care nurse is a licensed
professional nurse who is responsible
for ensuring that acutely and critically ill
patients and their families receive
optimal care .
Nurse Competencies

 Clinical Judgment
 Advocacy/moral agency
 Caring practice
 Collaboration
 Systems thinking
 Response to diversity
 Clinical inquiry
 Facilitator of learning
Critical care unit
 is a specially designed and equipped
facility staffed by skilled personnel to
provide effective and safe care for
dependent patients with a life
threatening problem.
THE AIM OF THE CRITICAL
CARE
 is to see that one provides a care such
that patient improves and survives the
acute illness or tides over the acute
exacerbation of the chronic illness.
THE EVOLUTION OF CRITICAL
CARE
 Forty years of development in critical
care and critical care nursing has given
rise to a recognized specialty in nursing
practice .
 Critical care units have evolved over the
last four decades in response to medical
advances .
HISTORICAL PRESPECTIVES
 Florence nightingale recognized the need to
consider the severity of illness in bed
allocation of patients and placed the seriously
ill patients near the nurses’ station.

 1923, John Hopkins University Hospital


developed a special care unit for neurosurgical
patients .

 Modern medicines boomed to its higher ladder


after world war 2
HISTORICAL PRESPECTIVES
 As surgical techniques advanced it became
necessary that post operative patient required
careful monitoring and this came about the recovery
room.

 In 1950, the epidemic of poliomyelitis necessitated


thousands of patients requiring respiratory assist
devices and intensive nursing care.

 At the same time came about newer horizons in


cardiothoracic surgery, with refinements in
intraoperative membrane oxygen techniques.
HISTORICAL
PRESPECTIVES
 In 1953, Manchester Memorial Hospital
opened a four bedded unit at
Philadelphia was started.

 By 1957, there were 20 units in USA


and

 In 1958,the number increased to 150.


Medical staff
 Intensivists are the best senior medical
Staff to be appointed to the ICU. He/she
will be the director. Less preferred are
other specialists from Anesthesia,
medicine and chest

 Junior staff are intensive care trainees and


trainees on deputation from other
disciplines.
NURSING STAFF
 The major teaching tertiary care ICU will require
trained nurses in critical care. It may be ideal to
have an in house training program for critical Care
nursing.

 The number of nurses ideally required for such


units is 1:1 ratio.

 The number of trained nurses should be also


worked out by the type of ICU, the workload and
work statistics and type of patient load.
UNIT DIRECTOR
 Specific requirements : Training,
interest, and time availability to give
clinical, administrative, and educational
direction to the ICU.
 Board certification in critical care
medicine.
 Time and commitment to maintain active
and regular involvement in the care of
patients in the unit.
UNIT DIRECTOR
 Availability to the unit 24 hrs a day, 7
days a week for both clinical and
administrative matters.

 Active involvement in local and/or


national critical care societies.
UNIT DIRECTOR
 Participation in continuing education
programs in the field of critical care
medicine.
 Active involvement as an advisor and
participant in organizing care of the
critically ill patient in the community as a
whole.
 Active participation in the education of unit
staff. Active participation in the review of
the appropriate use of ICU resources in the
hospital.
NURSE MANAGER
 An RN (registered nurse) with a BSN (bachelor of science in
nursing) or preferably an MSN (master of science in nursing) degree

 Certification in critical care or equivalent graduate education At least


2 yrs experience working in a critical care unit

 Experience with health information systems, quality


improvement/risk management activities, and healthcare economics

 Ability to ensure that critical care nursing practice meets appropriate


standards .

 Preparation to participate in the on-site education of critical care


unit nursing staff
NURSE MANAGER
 Ability to foster a cooperative atmosphere with regard to
the training of nurses, physicians, pharmacists,
respiratory therapists, and other personnel involved in
the care of critical care unit patients

 Regular participation in ongoing continuing nursing


education

 Knowledge about current advances in the field of critical


care nursing

 Participation in strategic planning and redesign efforts


Critical Care Unit Nursing
Requirements
 All patient care is carried out directly by or under
supervision of a trained critical care nurse.

 All nurses working in critical care should complete a


clinical/didactic critical care course before assuming
full responsibility for patient care.

 Unit orientation is required before assuming


responsibility for patient care.

 Nurse-to-patient ratios should be based on patient


acuity according to written hospital policies.
Critical Care Unit nursing
requirements
 All critical care nurses must participate in continuing
education.

 An appropriate number of nurses should be trained


in highly specialized techniques such as renal
replacement therapy, intra-aortic balloon pump
monitoring, and intracranial pressure monitoring.

 All nurses should be familiar with the indications for


and complications of renal replacement therapy.
RESPIRATORY CARE
PERSONNEL REQUIREMENTS
 Respiratory care services should be available
24 hrs a day, 7 days a week.

 An appropriate number of respiratory therapists


with specialized training must be available to
the unit at all times.

 Therapists must undergo orientation to the unit


before providing care to ICU patients.
RESPIRATORY CARE
PERSONNEL REQUIREMENTS
 The therapist must have expertise in the use of
mechanical ventilators, including the various
ventilator modes.

 Proficiency in the transport of critically ill patients


is required.

 Respiratory therapists should participate in


continuing education and quality improvement
related to their unit activities.
PHYSICIAN SUBSPECIALISTS
 General surgeon or trauma surgeon
 Neurosurgeon Cardiovascular surgeon
 Obstetric-gynecologic surgeon
 Urologist
 Thoraco-Vascular surgeon
 Anesthesiologist
 Cardiologist
 Pulmonologist
PHYSICIAN SUBSPECIALISTS

 Gastroenterologist
 Hematologist
 Infectious disease specialist
 Nephrologist
 Neurologist Orthopedic surgeon
 Physiotherapists prevents and treat chest
problems, assist mobilization, and prevent
contractures in immobilized patients
 Pharmacists advise on potential drug
interactions and side effects, and drug dosing
in patients with liver or renal dysfunction
 Dietitians Advise on nutritional requirements
and feeds
 Microbiologists Advise on treatment and
infection control
 Medical physics technicians Maintain
equipment, including patient monitors,
ventilators, hemofiltration machines, and blood
gas analyzers
OTHER PERSONNEL
A variety of other personnel may contribute
significantly to the efficient operation of the ICU.
 Unit clerks
 physical therapists
 occupational therapists
 Advanced practice nurses
 Physician assistants
 Dietary specialists
 Biomedical engineers.
LABORATORY SERVICES

 A clinical laboratory should be available on a


24-hr basis to provide basic hematologic,
chemistry, blood gas, and toxicology
analysis.

 Laboratory tests must be obtained in a timely


manner, immediately in some instances.
"STAT" or "bedside" laboratories adjacent to
the ICU or rapid transport systems.
Radiology and Imaging Services

 The diagnostic and therapeutic radiologic


procedures should be immediately
available to ICU patients, 24 hrs per day.

 Portable chest radiographs affect decision


making in critically ill patients.
ORGANIZATION OF ICU
 It requires intelligent planning.

 One must keep the need of the hospital and


its location.

 An institute may plan beds into multiple units


under separate management by single
discipline specialist medical ICU, surgical
ICU, CCU, burns ICU, trauma ICU, etc.
DEFINITION OF INTENSIVE CARE
UNIT EQUIPMENTS

 Intensive care unit (ICU) equipment includes


patient monitoring, respiratory and cardiac
support, pain management, emergency
resuscitation devices, and other life support
equipment designed to care for patients who
are seriously injured, have a critical or life-
threatening illness, or have undergone a
major surgical procedure, thereby requiring
24-hour care and monitoring.
Mechanical Ventilators
Syringe pump
Hemodialysis
Machine
Lifter
Swan Ganz Catheter
ICP Monitor
Ventriculoperitoneal Shunt
Sengstaken-blakemore tube
Salem-sump Tube
Levine Tube
Gastrostomy tube (G-tube)
Paracentesis
Tracheostomy and Endotracheal Tube
Chest Tube
Urinary catheter/tube
Colostomy
Wound Drains
Common Problems Seen in Critical Care Setting

1. Anxiety
2. Impaired communication
3. Sleep deprivation
4. ICU psychosis

Common procedures
1. Hemodynamic monitoring
2. Circulatory assist device IABP
3. Artificial Airway
4. Mechanical Ventilator
Complications

1. Sepsis
2. Multiple Organ System
Failure
3. Shock
Nursing Interventions

1. Anxiety related to fear of death, unknown patients and


significant others; ineffective coping mechanism .

Tx: Family participation, biobehavioral intervention

2. Impaired communication related to barriers : ET ,


newTT, or trauma
Tx : Acknowledge patient’s concern ; reassurance ;
alleviate common difficulties; family feedback
3. Sleep deprivation : lack of consistent REM and NREM

Tx: Meds ;Family visits ; rest periods; decreased


environmental stimulation

4. ICU psychosis

-acute confusional state sec.to CNS stimulants, narcotics,


depressants, steroids/ sleep deprivation, sensory overload,
F/E imbalance, dec. Oxygen, infection, head trauma, brain
disorders
Hemodynamic Monitoring
. Cardiac Output – volume of blood that is ejected from
the heart in 1 minute.
- determined by the HR x SV expelled per heart beat.
- NV- 4-8L/min.
. Pre-load – amount of stretch in the LV just before
ventricular contraction at the end of diastole.
. Afterload – tension the ventricle must overcome to eject
the blood into the arterial systems (pulmonary and aortic);
measured by the systemic vascular resistance.
. Cardiac index – is the CO by the BSA
- better indicator of the body’s ability to perfuse the tissues
effectively than CO.
- NV- 2.5 – 4.0 L/min/m 2
Types of Hemodynamic Monitoring

. Arterial lines – provides a direct, intra-arterial measurement


of BP; assist in the continuous measurement of SBP, DBP
and MAP.

Method : a 20 g arterial catheter inserted into the radial,


brachial or femoral artery connected to high pressure
tubing leading to a pressure transducer and amplifier.
Nursing Management : Same mechanics in CVP
reading
1. Drawing a – blood sample – flush A line with valve flush
device to allow return of sharp arterial waveform thru a 3
way stopcock.
2. Change dressings 24-48 hrs., IV solutions and IV tubings
per hosp. policy 48-72 hrs.
3. Watch out for complications : bleeding from insertion site ,
hemorrhage, infection- systemic , air embolus, thrombosis,
occlusion of circulation with loss circulation distal to
insertion site.
4. Perform Allen Test prior to radial artery insertion and freq.
monitor distal pulses.
2. Swan-Ganz Catheter – Pulmonary Artery Balloon Flow
provide indirect measurement of LV function for detection
and treatment of CP changes.

Method : a 5 lumen, balloon tipped , flow directed catheter


connected to a pressure transducer and pressurized
heparin flush system is inserted thru a percutaneous
or cutdown venous site and directed into the RA.

Site : subclavian vein most common


Indications :

a. a need to monitor PAP and or PCWP- indirectly


reflect LV function.
b. provide information about CO, tissue perfusion
and BV.
c. Obtain venous blood specimens
d. Proximal orts used for continuous fluid or
medication infusion.
Nursing Management :

1. Level and secure transducer at the phlebostatic axis –


4th ICS, MAL – serves as a reference point for the RA.
2. Taking readings – record PA Systolic and Diastolic
Pressures to obtain a PCWP or LVEDP , then inflate
the catheter balloon slowly, watch for waveform
changes-dampening indicates wedging.
3. After reading has been recorded, allow the balloon to
deflate passively and lock it out tp prevent accidental
wedging- take all reading at the end of expiration.
4. W/O for complications : dysrrhythmias, infection, air
embolism,catheter occlusion, pneumothorax, thrombus
formation.

3. Circulatory Assist Device – Intra-Aortic Balloon Pump


a counterpulsation device that assists to augment CO and
to provide adequate rest and recovery.
Indications :
cardiogenic shock
heart failure
support before heart transplantation
unstable angina
failure to wean from CP bypass after coronary
bypass surgery
Nursing Management :

1. Assist with placement as needed and maintain sterilit


with dressing changes.
2. Monitor and record effectiveness – inc. CO, inc. BP,
inc. U.O., inc. LOC, palpable peripheral pulses,
improved ischemic EKG changes.
3. Monitor circulation, sensation and motor function in leg
of insertion , keep the affected leg straight at all times.
4. Keep HOB elevated at least 30 degrees to prevent migration
of the balloon.
5. Monitor Sx : hematuria ( excessive anti coagulants )
excessive oozing from catheter insertion
sites
positive guiac in the stool
abnormal PT,PTT and platelet counts
6. Complications : air/foreign body embolus if balloon
should rupture
thrombus formation at insertion site
loss of distal circulation
migration of catheter
dissection of aorta
sepsis
complications of immobility
Common Complications in the ICU :

SEPSIS

-a diffuse, inflammatory systemic response to a chemical,


mechanical, bacterial or microbial assault if untreated
leads to shock.
-Severe sepsis : hypoperfusion,organ dysfunction,
hypotension, septic shock, multi organ systemic failure,
death.
Management :

1. ABC
2. D- disability/ drugs : Inotropics, Vasodilators
3. E-expose : V/S : CVP, ECG
4. F-fluids , nutrition
5. anti pyretics/antibiotics

MOSF

Cause : failure of one or more body systems after a major


insult to the body such as infection, trauma, severe
illness, persistent hypotension and hypoxia.
4 Major Systems :

1. Pulmonary dysfunction
2. Renal dysfunction
3. CV dysfunction
4. Coagulation system failure

S/Sx: per organ dysfunction leads to dec. LOC then coma


with bleeding and fibrinolysis.
Dx; 1. ABG- severe acidosis
2. WBCs – dec. platelet less than 80,000/mm 3
3. dec. fibrinogen
4. inc. PT,PTT, hgb, hct , severe anemia
5. inc. urea, BUN
6. inc. cardiac, hepatic enzymes
7. inc. serum K
8. CXR – interstitial edema and hypoperfusion
Tx:
1. V/S,CVP 8-10 mmHg
2.ABC
3. Hemodialysis
4.Nutritional suspport
5. Antibiotics
6.Bleeding control
7.Limit activities

SHOCK
-a state of imbalance between O 2 supply and demand in the
body that leads to inadequate blood flow to organs, poor
tissue perfusion- possibly fatal cellular dysfunction.
Classification:

1. Loss of CBV – hypovolemic


2. Dec. pump function – cardiogenic
3. Spinal cord injury – Neurogenic
4. Overwhelming presence of endogenous
mediators causing inflammatory response
– septic

Compensatory Mechanisms :
1. SNS- massive release of NE
2. Endocrine -ADH
S/Sx :

Early Stage : normal BP, slightly increase CR, normal to


slightly dec.U.O., slight restlessness, anxiety,
thirst
Next Stage : progressive shock state – claasic shock sx ;
cool clammy pale skin, dec. capillary refill,
tachycardia, tachypnea, dec. BP, CO, temp.,
U.O., LOC, metabolic acidosis
Later Stage : Sx of specific organ failure : anuria, slow
thready pulse, ARDS, bleeding, coagulation
dysfunction, coma.
Dx:

1. dec. hgb/hct
2. ABG- acidosis
3. inc. serum lactate and K
4. inc. cardiac hepatic GI enzymes
5. inc. BUN crea – RF
6. initially increase glucose to decrease glucose stores
7. dec. sp. grav. urine
8. depletion of clotting studies
9. ST ischemic changes ECG
Management :

1. ABCDEFGH
2. BT.IV NSS, LR, O 2, Vasopressors, vasodilators,
inotropics
3. Correct acidosis- anaphylactic and septic shock
4. Comfort measures
5. V/S,UO,,peripheral circulation, titrate meds., thorough
assessment
6. Cardiac dysrythmias, coagulation dysfunction, I^O,
hemodynamic status
7. dec. external stimuli, family teaching
ARDS Acute RDS

-a syndrome char. by a non-cardiac type of pulmonary


edema and increasing hypoxemia despite administration
of tx measures formerly known as adult resp. distress
syndrome.
S/Sx :
1. labored respirations
2. restlessness
3. dry, non productive cough
4. cyanosis
5. pallor
6. adventitious breath sounds with used of
accessory muscles with retraction
Dx :
1. CXR – white out due to bilateral diffuse infiltrates
2. PFT – dec. in compliance , lung capacity
3. Increase peak inspiratory pressures
4. ABG- initially resp. alkalosis due to hyperventilation
then acidosis.
5. Inc. hemodynamic monitoring – PA Systolic and
Diastolic Pressures with normal PAWP.
Pathology :

1. Primary Insult
2. Chemical mediators released
3.Interstitial edema
4. Alveolar edema
5. Damaged surfactant producing cells
6. Dec. lung compliance
7. Atelectasis, hyaline membrane formation
8. Inc. work of breathing
9. Impaired gas exchange
10. Respiratory failure
Tx :
1. O2
3. Sedation to tolerate mech. Ventilation
4. Fluid therapy- crystalloids, colloids – IVC volume
5. Hemodynamic monitoring
6. Treat underlying cause of ARDS- antibiotics
7. Provide nutritional support – CHON balance
8. Steroid therapy – stabilize cellular membrane and dec.
fluid shifts
9. Diuretic therapy
10. Comfort, positioning HOB elevated
11. V/S, EKG, Neuro
12. Conserve energy-schedule activities/family teaching
CARDIOPULMONARY RESUSCITATION

BCLS – to recognize cardiac or resp. arrest and re establish


or provide airway breathing pattern and effective
circulation until the client responds or until another
type of life support is initiated.
HT / CL maneuver, jaw thrust maneuver LLF
M-M/ ambu bag
Closed CC
Adult one rescuer: 15:2 for 4 cycles : 1 minute
1 ½ inches compression lower 1/3 sternum at a rate of 100
times per minute.
ACLS – manages the airway thru ET intubation or use
of an advanced airway device.

- ET placement check
- Venous access peripheral IV g 16-18
Drugs:
ibrillation, Pulseless Vtach :

1. Epinephrine 1mg repeated 3-5 min, IV; tracheal adm.


2-2.5mg in 10 ml NSS
2. Vasopressin –Pitressin 40 U or ET single dose once only
3. Amiodarone- Cordarone 300mg IV
4. Lidocaine-Xylocaine-1-1.5mg/kg IV
5. Lidocaine drip 1-4 mg/min for maintenance infusion
6. Procainamide 20mg/min IV
7. Na HCO3- 1 MEQ/kg/IV bolus
Asystole: pulseless electrical activity
1. Epinephrine
2. At SO 4
3. CPR/ transcutaneous pacing
Bradycardia
1. At SO 4

Ventricular fibrillation
-chaotic rhythm, rapid disorganized depolarization of
ventricles

Tx: defibrillation – 200-300-360 joules / O 2 / CPR /


Epinephrine lidocaine amniodarone
Ventricular Tachycardia

-rapid ventricular contraction 100bpm above


VR – 150-250 bpm QRS more than .12 sec. wide, bizarre

Tx : hemodynamically stable: O 2 / lidocaine amniodarone


to dec. irritability
PVC
-ectopic beats occur earlier than expected followed by a
compensatory pause.
Salvos:
1. more than 6/min PVC
2. paired
3. multifocal –differing shapes
4. R on T

Tx: Lidocaine
SVT

-more than 100 bpm originating above the ventricle but


not in the sinus node.
-AR more than 140 bpm VR depends on degree of block

Tx :

1. Attempt vagal nerve stimulation


2. Adenosine 6 mg rapid IVP
3. Verapamil – Isoptin 2.5-5mg Iv over 2 mins.
4. Synchronized Cardioversion
Nursing Role During a Code :

Call Code
CPR, paraphernalia
Determine team leader
Serial assessments and documentation
Crowd control
Psychosocial needs of family, room mates and staff
Diabetic Ketoacidosis

-a complication of IDDM, a condition arising from a lack of


insulin resulting in a derangement of CHO, CHON and fat
metabolism with DHN and electrolyte imbalance.

Ketoacidosis occurs when FA are broken down to ketone


bodies because of absoloute or relative deficiency of insulin.
Etiology : As the need for cellular fuel grows more critical ,
the body begins to draw on its fat and CHON
stores for energy.
 Increase fatty acids are metabolized from
adipose tissue cells and transported to the liver.
 Liver in turn, accelerates the rate and produces
ketone bodies ( KETOGENESIS ) for catabolism
by other body tissues particularly muscle.
 As increase metabolism- increase ketone
bodies – accumulate in the blood
 ( KETOSIS ); spill into urine ( KETONURIA );
metabolic acidosis develops develops from
acidic effect of ketoacetoacetate and B-
hydroxybutyrate---- severe acidosis
Precipitating Factors :

1. taking too little insulin


2. omitting doses of insulin
3. failing to meet increased for insulin due to surgery,
trauma pregnancy puberty or febrile illness.
4. developing insulin resistance owing to insulin
antibodies or severe emotional stress.
4 Pathologic events in DKA
1.Incomplete lipid metabolism
2. DHN
3. Metabolic acidosis
4. Electrolyte imbalance
S/Sx :
 - hyperglycemia
 glycosuria
 polydipsia
 ketonemia
 ketonuria
 metabolic acidosis
 Kussmaul’s respiration
 acetone breath-dec. acetone combining power
 DHN
 dry skin
 sunken eyeballs
 flushed face
 electrolyte imbalance
 tachycardia
Management : Prevent complications

1. Adequate ventilation
2. Fluid replacement-NaHCO3,NaCl,K
3. Insulin
4. Indwelling FC
5. IVF,D5050 IV
6. Hgt ,ABG,CXR,12 lead EKG
HHNK- Hyperglycemic Hyperosmolar
Nonketotic Coma

-a condition resulting from elevated concentration of blood


glucose

- level which increases the osmolarity of blood without


significant ketoacidosis.
Causes :

1. large NaHCO3 infusion as in CPR


2. marked hyperglycemia
3. uremia with increased BUN
4. Na retention from adrenal steroid

Tx:
1. Insulin
2. F/E
3. Dialysis
S/Sx:

1. increased temp. 41 C
2. DHN
3. irritability
4. frustration
5. cardiac dysrythmias
6. CHF
7. delirium
8. diarrhea/N/V
RENAL FAILURE

-state of total or nearly total loss of the kidney’s ability to


maintain F/E balance and excrete waste products.
-inability of the kidney to function normally or effectively.
Renal Insufficiency
-designates significant loss of renal function but with
a function requiring to maintain a normal environment
provided no additional stress is added.

Azotemia
-accumulation of nitrogenous wastes within the blood,
not life threatening without a decreased output.

Uremia
-an azotemia progressing to a symptomatic state.
Types of Renal Failure :

A.Acute RF

-a sudden, complete or nearly complete loss of kidney


function which develops rapidly over a period of day or
few weeks. Output drops suddenly to less than 400ml/day.
3 Phases :

1.Oliguric Phase – begins shortly after injury and is char.


By gradually decreasing U.O.
2.Anuric Phase – there is total absence of urine production.
3. Polyuric Phase – recovery , there is marked diuresis,
there may be rather marked wasting of various
electrolytes, esp. Na, K, HCO3.
Causes :

1. Pre-renal – when the lesion or cause is before the kidney.


- shock, mismatch BT
2. Renal – when the lesion is found in the kidney itself.
- nephritis,nephrotoxic infection
3. Post renal – reached the kidney
- obstruction of the urinary tract : renal calculi.
B. Chronic RF
-gradual deterioration of kidney function
occurring over months or years.

3 Stages:
1. Stage of diminished renal reserve- renal function is
impaired but metabolic wastes do not accumulate in
the blood and the BUN remains normal.
2. Stage of renal insufficiency – metabolic wastes begin
to accumulate in the blood and there is a slight increase
in BUN.

3. Stage of uremia – the kidney loses its ability to maintain


homeostasis.U.O. is usually scanty, electrolyte balance
is severely disturbed and nitrogenous wastes accumulate
in high concentrations.
3 Causes :

1. Pre-renal
-gout,DM,sub acute endocarditis
2. Renal
-SLE,pyelonephritis,GN
3.Post renal
-prostatic obstruction
S/Sx :
 alteration in U.O.
 weak,easily fatigued becomes increasingly drowsy
 HA and slight breathlessness and lethargic
 restlessness and insomnia
 dry, skin and mucous membrane
 halitosis- urineferous breath
 loss of appetite, intractable N/V
 CNS manifestation- anxiety, irritability, hallucination,
mental wandering, muscle twitching, coma
 HPN
 anemia
 edematous, tend to bruise easily
Management :

1. Diet: dec. CHON,


essential amino acid, -controlled K 1,500mg, 20g
very low CHON, minimal essential AA.
2. Tx of Infection : unnecessary surgery and instrumentation
are avoided; antibiotics
3. Tx of alterations in Body Chemistry
-limit CHON metabolism and K ;
-hyperkalemia –peaked T wave, depressed ST segment,
flaccid paralysis,slow respiration, anxiety, convulsions

Tx: Kayexalate –contain Na in a compound absorbed


by the GIT. While in the GIT, the Na exchange places
with serum K ; and K becomes part of the non absorbable
compound.
-Ca gluconate- as an emergency measure when the K level is
dangerously high and cardiac arrythmias are imminent.

-Glucose and insulin- insulin causes glucose to go into cell; as


glucose moves into the cell, it takes with it and reduce the
serum K.

-Na HCO 3 – treat acidosis.


Aggressive Mgmt :

1. Hemodialysis
2. Peritoneal Dialysis
THANK YOU!

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