http://www.doh.gov.

ph/chdncr/images/pdf2/a%20suspect%20meningococcemia
%20case.pdf

Subject: Reported death from Meningococcemia at The Medical City last Dec. 9,
2006

______________________________________________________________________

Introduction: On December 10, 2006, the Regional Epidemiological and Surveillance

Unit (RESU) was informed by Mrs. Vicky Ching, Infection Control Nurse of Medical
City,

of a patient who died of Meningococcemia several hours after admission at The

Medical

City Hospital. Coordination with Dr. Rolando Paac, City Health Officer of Taguig City,
Dr.

Jun Palma and Ms. Daisy Bulacan, surveillance officers of the City Epidemiological
and

Surveillance Unit (CESU), Dr. Alzona, Rural Health Physician in Napindan, Mr. Victor

Ong, owner of Paulinian Pawnshops and Mr. Mario Esguerra, Barangay Captain of

Napindan was done.

Methods: The RESU interviewed the husband and other members of the family of
the

deceased. Review of medical records at The Medical City and contact tracing were

conducted. Review of Meningococcemia cases and deaths in Napindan, Taguig

during

the past year was also done.

A Suspect Meningococcemia case is one who developed sudden onset of fever

>38C

with at least one of the following: neck stiffness, altered consciousness, bulging

fontanelles in infants and non-blanching purpuric or petecchial rashes. A Clinically

confirmed Meningococcemia case is a suspect case with acute fever, in shock and

with rapidly progressing rash with no laboratory diagnosis done or questionable

laboratory result. A Laboratory-confirmed Meningococcemia case is one who

obtained positive result from one of the following tests: isolation of N. meningitides
from

a sterile site, blood or CSF; identification of N. meningitides DNA from the sterile
site,

blood or CSF; and positive latex agglutination for N. meningitidis in the CSF.

Findings: CL was 39 years old, Female, Married, childless and a resident of 7 D. Labo

St. Napindan, Taguig. She was connected with three Paulinian Pawnshops located at

Rosario and San Joaquin, Pasig and Antipolo City.

Last December 7, 2006, she came home from work with complaints of severe
headache,

throat pain, cough and colds. No medication was taken. Patient thought she had

influenza.

The following morning, she had fever, headache and vomiting (about ten times). A
few

hours before she was brought to The Medical City, she was still febrile, looking very

weak, restless and disoriented. Appearance of multiple erythematous macules and

patches were noted on the arm and shoulder. The relatives thought she had dengue

fever and so they decided to bring her to the hospital, The Medical City.

Patient was a known asthmatic. She had her last attack of asthma last Nov.2006.
She

had no history of trauma involving the head or any part of the body.

On physical examination, patient was tachycardic (138/min) and hypotensive (70/

50).

Conjunctival suffusion, dried lips and tongue, nuchal rigidity and generalized
petechial

and purpuric rashes were noted. Admitting diagnosis was Meningococcemia, with

Meningococcal Meningitis Patient was given IVF and parenteral antibiotics. A few
hours before death, she was

noted to be lethargic and disoriented. Patient expired at about 2:26 PM of Dec. 9.

Final
Diagnosis was Meningococcemia with Meningococcal Meningitis.

Significant laboratory results were: elevated WBC count (23,000/ cu.mm) and

Neutrophils (0.85) and presence of toxic granues; elevated creatinine level, low
sodium

level,. Culture of the blood sample revealed growth of N. meningitides.

The corpse was buried on Dec. 11 (12:00 PM), two days after her death because the

relatives refused early burial due to financial constraints. However, the Taguig City

Health Office facilitated immediate burial of the corpse at a Catholic Cemetery.

Last year’s surveillance data revealed no reported case or death from

Meningococcemia

in Napindan, Taguig.

Discussion: CL is a Laboratory-confirmed case of Meningococcemia. Confirmation

was based on the result of the blood culture (growth of N. meningitides) which was
done

at The Medical City. Rapid deterioration of the patient’s condition was very
evident.

Patient developed shock early and then expired on the second day of the illness.
The

source of the infection was undetermined since she had no exposure to a known

meningococcemia case. She could have gotten the infection from a carrier.

Chemoprophylaxis was given to fourteen close contacts- ten family members of CL

and

four neighbors who assisted her during transport to the hospital. Seven co-
employees

(including the employer) in the three pawnshops where she worked and the four
staffs of

De Guzman Funeraria were also given chemoprophylaxis. Chemoprophylaxis

against

meningococcemia is very crucial since this will prevent the occurrence of the
disease
among the contacts as well as eliminate the carrier state. All the identified contacts
will

be monitored for two weeks for any development of signs and symptoms of

meningococcemia.

Meningococcemia is the leading cause of meningitis and rapidly fatal sepsis in

otherwise

healthy individuals. In endemic countries, 5-10% of the population is asymptomatic

carriers. Case Fatality Rate (CFR) is 5-15% for those diagnosed and treated early.
On

the other hand, CFR exceeds 50% with late treatment. CFR for meningococcemia

without meningitis is 25% more as compared to meningococcal meningitis. The

causative agent is Neisseria meningitidis, gram-negative diplococci that colonizes

the

oropharynx and nasopharynx of asymptomatic carriers. The organisms do not

survive

well outside the human host. Transmission is thru direct contact with contaminated

respiratory secretions or inhalation of infected droplets from a known infected case

or

close direct physical contact with an infected carrier. Incubation period is from 2 –
10

days, commonly 3-4 days. Clinical features are sudden onset of fever, intense

headache, nausea and vomiting, stiff neck, petecchial rash with pink macules,

ecchymoses, shock, delirium, coma and death. It can progress to invasive disease
such

as bacteremia, septicemia, meningitis and pneumonia. Actions Taken by:

The Medical City:

1. Chemoprophylaxis of family contacts (10) with Ciprobay

2. Chemoprophylaxis of medical staffs who had direct contact with the deceased

Taguig City Health Office:

1. Strengthening of Meningococcemia surveillance in Napindan, Taguig City

2. Chemoprophylaxis of other close contacts in the community

3. Information education on Meningococcemia

4. Immediate burial of corpse at a Catholic Cemetery in Taguig

By the CHD – MM RESU:

1. Coordination with the RHU of Napindan regarding setting up of

Meningo-surveillance

3. Coordination with Ms. Raquel Havana, Surveillance Officer of Pasig City

Epidemiological and Surveillance Unit for setting-up of Meningo-surveillance in

the two areas where the two pawnshops are located.

4. Coordination with Mr. Dante de Guzman for chemoprophylaxis of embalmers of

the deceased

5. Coordination with Mr. Victor Ong, employer of Paulinian Pawnshop, for

chemoprophylaxis of other contacts in the three pawnshops.

6. Distribution of health advisories on Meningococcemia

Written by: DR. ANTHONY Z. SAN JUAN

Epidemiologist

http://findarticles.com/p/articles/mi_m0906/is_n3_v40/ai_10381246/

Laboratory-Acquired Meningococcemia -- California and Massachusetts

Although Neisseria meningitidis is commonly isolated in clinical laboratories,

laboratory-acquired infection is rare (1). This report describes two fatal cases
of meningococcal infection in laboratory workers both of these cases
probably were laboratory acquired.

Case 1. On March 8, 1988, a clinical laboratory bacteriologist in California

became ill with influenza-like symptoms and nausea. During the next 24
hours, she developed fever, myalgias, arthralgias, diarrhea, skin lesions, and
confusion. Her husband informed ambulance personnel that she had had a
mishap in the laboratory approximately 1 week earlier with a type of
organism that causes meningitis.

When hospitalized at 10 p.m. on March 9, she was hypotensive with

numerous petechial and purpuric lesions on her face, neck, trunk, and
extremities she died 6 hours later. The final autopsy diagnosis was "clinical
acute intractable shock, consistent with acute meningococcemia." Blood
cultures and cerebrospinal fluid studies were negative. Serum was positive
by a bivalent (groups C and W135) latex agglutination test for N.
meningitidis. A throat culture grew N. meningitidis.

No mishap had been reported at the hospital laboratory where the patient
worked, nor could the patient's co-workers recall any episode no additional
information regarding a mishap could be discovered. During the previous 3
months, the patient worked with only one known N. meningitidis isolate,
which was obtained from the blood of a patient with acute meningitis and
cultured by the affected laboratory worker 5-6 days before onset of her
symptoms. Both the workplace isolate and the laboratory worker's
nasopharyngeal isolate were identified as N. meningitidis serogroup C by the
Microbial Diseases Laboratory of the California Department of Health
Services.

CDC performed isoenzyme testing on the laboratory worker's

nasopharyngeal isolate, the workplace isolate, and 14 other unrelated but
recently isolated group C strains from throughout northern California. The
isoenzyme type of the laboratory worker's isolate and the workplace isolate
were identical and rare. They differed from the 14 northern California
isolates (p 0.01, Fisher's exact test) and from a collection of 256 group C
meningococci isolated between 1986 and 1989 (p 0.01, Fisher's exact test).

Case 2. On the morning of September 6, 1988, a microbiology technician at a

teaching hospital in Massachusetts presented to the hospital's employee
health clinic with a history of several days of rhinorrhea, sore throat, and
myalgias. She was sent home at 1 p.m. with a diagnosis of viral syndrome.
Twelve hours later, she presented to the emergency room semiresponsive,
hypotensive, dyspneic, and with petechial and purpuric skin lesions. A gram
stain of the buffy coat of her blood showed gram negative diplococci. Despite
antibiotic therapy, she died 6 1/2 hours later. Blood cultures grew N.
meningitidis group B.

For several days before her hospitalization the patient had been working in
the bacteriology laboratory at the teaching hospital despite her upper
respiratory infection symptoms. The laboratory had not isolated N.
meningitidis during the 3 weeks before the patient's illness. On September 3
and 4, the patient worked in the bacteriology laboratory of another hospital.
She had been observed using gloves to subculture an N. meningitidis isolate,
and she had extensive rhinorrhea.

Both the workplace isolate and the patient's blood culture isolate were
identified as N. meningitidis serogroup B. Isoenzyme testing performed by
CDC on the patient's blood isolate, the workplace isolate, and nine other
unrelated but recently isolated group B strains from Massachusetts
demonstrated that the isoenzyme pattern of the patient and workplace
isolate were identical. They differed from the nine other Massachusetts
group B isolates (p 0.02, Fisher's exact test).

Editorial Note: Laboratory-acquired infection with N. meningitidis is rare.

Three previous case reports describe infections in persons working in
research laboratories who handled meningococcal organisms frequently and
in large volumes (1,2) two of these occurred before the availability of
effective vaccines and antibiotic therapy.

Although N. meningitidis was never isolated from the blood of the laboratory
worker in California, other evidence supports the conclusion that she had
laboratory-acquired meningococcal infection. The worker in Massachusetts
may have been at increased risk for meningococcal infection several studies
suggest that concurrent viral infection increases the risk of developing
invasive meningococcal infection [3-5!.

These cases represent the first reports of meningococcal infection acquired

in the clinical laboratory setting. Although laboratory workers frequently
handle specimens and cultures containing meningococci, the laboratory
workers probably are not at increased risk of infection when standard
microbiologic practices are followed.
Opisthotonus

Brudzinski

Kernig’s

http://books.google.com.ph/books?
id=cgJRTdOcuB8C&pg=PA134&lpg=PA134&dq=meningococcemia+case+study&so
urce=bl&ots=rp-
9yfEeBl&sig=vd9Mvini7WyF1ByaPWpVrehyq8A&hl=tl&ei=x7wNTbbGEoj5ca-
i7NwK&sa=X&oi=book_result&ct=result&resnum=3&ved=0CCYQ6AEwAjgU#v=one
page&q=meningococcemia%20case%20study&f=false

A 10-year-old boy presents with meningococcemia. He has a 24-hour history of

fever, increasing lethargy, and a rapidly progressive petechial rash. He has had no
urine output in 12 hours. His vital signs are as follows: temperature, 103 F; heart
rate, 140 beats/min; blood pressure 70/30 mm Hg; and respiratory rate, 40
breathes/min with obvious hyperpnea. On physical examination, the patient is
lethargic but arousable. His skin examination reveals a diffuse petechial rash that is
becoming purpuric in the groin region. His capillary refill time is 4 to 5 seconds.

Laboratory data include the following: (1) complete blood count, with hemoglobin,
10 g/dL; hematocrit, 30%, white blood cell count, 2700/mm3 with 25 segmented
neutrophils, 40 bands, 20 lymphocytes, 12 monocytes, 2 eosinophils, and 1
basophil; and platelet count, 43,000/uL; (2) prothrombin time, partial
thromboplastin time, and fibrin degradation products, all elevated; (3) marked anion
gap metabolic acidosis; (4) liver enzymes elevated (80Os); and (5) blood urea
nitrogen and creatinine; elevated.

http://allnurses.com/general-nursing-student/nursing-diagnoses-meningitis-
367965.html

Lets say a patient has Bacterial Meningitis and these were some diagnoses. Which
one is the number one priority?
Acute Pain
FVD
High Risk for Injury
Risk for Ineffective Cerebral Tissue Perfusion
KD
Risk for Trauma/Suffocation
Hyperthermia
Risk for Infection

(1) FVD (2) Hyperthermia (3) Acute Pain (4)Risk 4 ineffective cerebral
tissue perfusion (5) High risk 4 injury (6) Risk for Trauma/Suffocation (7)
Risk 4 infection (8) KD Is this right?
No. I have sequenced them and given you my reasons below. Many of them are not
the current NANDA labels. Some are labels not even approved by NANDA. That
makes it difficult to determine priority, especially with Risk for
Trauma/Suffocation which is, on one hand, very vague (trauma) and, on the
other, very specific (suffocation--involving breathing and oxygen). I would never
compose a diagnosis like this.
1. Deficient Fluid Volume (physiological need for fluid)
2. Hyperthermia (physiological need for control of body temperature)
3. Acute Pain (physiological need for comfort)
4. Deficient Knowledge (safety need)
5. Risk for Ineffective Cerebral Tissue Perfusion (anticipated need for oxygen to
the brain)
6. Risk for Trauma/Suffocation (anticipated need for oxygen to the lungs--
trumps the anticipated need for protection)
7. Risk for Infection (anticipated need for physiological safety)
8. High Risk for Injury (anticipated need for protection)

http://allnurses.com/general-nursing-discussion/nursing-care-plan-343787.html
Well this patient came in just when she was feeling much better but her admitting
diagnosis was fever and altered mental status after labs and diagnostics
test(lumber puncture,x ray and CT scan) they resulted in nothing but she was
treated with ATB and also IV fluids all pushed thru a PCVC.Her vitals her bp
146/86,p 88,RR 18 POX 96% is denies any pain even though when she was
admitted she complained of HA and I have to assess her on her 6th day of
admission so obviously she was much improved so I am just feeding out of
information I got from the Dr's note,she is alert & orientedX2 earlier on but was
improved by day 6,so I don't really have much to go with since my patients
condition is improved and she was discharged after her completion of her ATB.Hope
this helps

http://wps.prenhall.com/wps/media/objects/354/362846/Child%20-
%20Bacterial.pdf

1. Deficient Fluid Volume (physiological need for fluid)

 2. Hyperthermia (physiological need for control of body temperature)
3. Acute Pain
4. Fear/ Anxiety

http://www.wpro.who.int/media_centre/press_releases/news_20050223.htm
WHO to help the Philippines investigate disease outbreak
Manila, 12 January 2005 - The World Health Organization (WHO) has offered its support
to Philippine health authorities in their investigation of suspected meningococcemia
cases in the northern tourist city of Baguio, where eight cases of the disease have been
confirmed since last October.

Dr Jean-Marc Olivé, WHO's representative in the Philippines, said the situation in the
Baguio area needed to be better understood, and more extensive investigations would
be needed to ascertain how serious a threat the disease was. "To help with these
investigations, we will initially be providing the services of laboratory and epidemiology
experts," Dr Olivé said. A command post has been set up in Baguio with WHO's
assistance to help with investigations and control.

In addition to the eight laboratory-confirmed cases, Philippine authorities have reported

25 suspected cases in Baguio since the beginning of 2004. A total of 19 people have
died. "This is an exceptionally high case fatality rate for meningococcal infection," said
Dr Olivé, "so we are treating the situation seriously. However, we need to know how
many of these suspected cases are really due to meningococcal infection and not to
other causes. By fully understanding the extent of the problem, additional appropriate
control measures can be undertaken."

Dr Olivé said there was no need for members of the public - from the Philippines or
from abroad - to avoid travel to Baguio. "There is a very low risk of infection among
travellers," he said. "The disease is spread only through very close contact, such as a
prolonged household setting. So there is little chance of infection in a normal public
setting." Dr Olivé added that produce from Baguio, such as fruit and vegetables, was
safe.

Meningococcemia is endemic in the Philippines and much of Asia, but rarely results in
large clusters. Most cases are sporadic in nature.

The infection presents as meningitis (meningococcal meningitis) or septicaemia

(meningococcemia) or a combination of both. The symptoms of meningitis are a
headache, vomiting, and a stiff neck, sometimes with a bruise-like rash. Septicaemia
symptoms are a spreading rash and fever, sometimes with signs of meningitis. The
infection is seasonal, with a higher incidence in the winter months. The incubation
period is 2-10 days.
The confirmed cases in Baguio have been identified as serogroup A, for which most
commonly available vaccines are effective. At this time, given the available information,
mass vaccination in Baguio is not recommended.

http://casesjournal.com/content/2/1/7103

http://www.who.int/csr/don/2005_01_11/en/index.html

http://findarticles.com/p/articles/mi_7490/is_20100112/ai_n52343187/

http://www.doh.gov.ph/programs/meningococcemia.html

Identification:This disease is also called meningococcal meningitis or cerebrospinal

fever. It is an acute disease caused by a gram negative bacteria Neisseria meningitidis.
The infection may be asymptomatic, may be restricted to the nasopharynx, or exhibit
upper respiratory tract infections. It may cause meningococcal septicemia, or
meningitis. Incubation period lasts for 2-10 days with an average of 3-4 days.

The disease is characterized by sudden onset of high grade fever (>380C) lasting for 24
hours. Other signs and symptoms are petechial and/or purpuric rashes appearing within
24 hours after onset of fever, and signs of meningeal irritation such as: headache,
nausea and vomiting, stiff neck, bulging fontanel (among infants), seizure or
convulsions, and sensorial changes.

Diagnosis: Diagnosis is confirmed by demonstration of the bacteria in a gram-stained

smear of the cerebro-spinal fluid (CSF) and the isolation of the bacteria from the CSF
blood.

Occurrence: The disease is usually sporadic (cases occur alone or may affect
household members with intimate contact). Although primarily a disease of children, it
may occur among adults especially in conditions of forced overcrowding such as
institutions, jails and barracks. It occurs more in males than females.

Mode of transmission: Transmission is by direct contact with respiratory droplets

from nose and throat of infected persons. Carriers may exist without cases of
meningitis. Transmission via inanimate objects (personal belongings of cases) is
insignificant.

Prevention and Control: Preventive measures are geared towards reducing

overcrowding and exposure to droplet infection. Immunization of civilians is not
recommended as duration of protection is limited.

Treatment and Prophylaxis: Treatment is effected by antibiotics and if given early,

fatality rate is rendered less than 10%. Aqueous Penicillin G may be given to both
children and adults. Chloramphenicol may be given in cases of Penicillin allergy.
Prophylaxis is reserved for those who have intimate contact with the patient; household
members, boyfriend/girlfriend, sexual partners, hospital personnel who did suctioning
of secretions and/or mouth resuscitation. Rifampicin is the drug of choice and may be
given to both children and adults.

http://www.online-health-care.com/diseases/meningococcal-infections.htm

http://www.ehealth.ph/index.php/latest-ehealth-news/25

http://findarticles.com/p/articles/mi_7490/is_20100112/ai_n52343187/

http://www.jpeds.com/article/S0022-3476(55)80180-1/abstract

http://casesjournal.com/content/2/1/7103

http://wps.prenhall.com/wps/media/objects/737/755395/septic_shock.pdf

http://www1.us.elsevierhealth.com/MERLIN/Gulanick/Constructor/index.cfm

NANDA Definition: Decrease resulting in the failure to nourish the tissues

at the capillary level
Reduced arterial blood flow causes decreased nutrition and oxygenation at
the cellular level. Management is directed at removing vasoconstricting
factor(s), improving peripheral blood flow, and reducing metabolic demands
on the body. Decreased tissue perfusion can be transient with few or
minimal consequences to the health of the patient. If the decreased
perfusion is acute and protracted, it can have devastating effects on the
patient. Diminished tissue perfusion, which is chronic in nature, invariably
results in tissue or organ damage or death. This care plan focuses on
problems in hospitalized patients.
Defining Characteristics:
 Peripheral:
 Weak or absent peripheral pulses
 Edema
 Numbness, pain, ache in extremities
 Cool extremities
 Dependent rubor
 Clammy skin
 Mottling
  Differences in blood pressure (BP) in opposite extremities
 Prolonged capillary refill
 Cardiopulmonary:
 Tachycardia
 Dysrhythmias
 Hypotension
 Tachypnea
 Abnormal arterial blood gases (ABGs)
 Angina
 Cerebral:
 Restlessness
 Confusion
 Lethargy
 Seizure activity
 Decreased Glasgow Coma Scale scores
 Pupillary changes
 Decreased reaction to light
 Renal:
 Altered blood pressure
 Hematuria
 Decreased urine output (<30 ml/hr)
 Elevated BUN/creatinine ratio
 Gastrointestinal:
 Decreased or absent bowel sounds
 Nausea
 Abdominal distention/pain
Related Factors:
 Peripheral:
 Indwelling arterial catheters
 Constricting cast
 Compartment syndrome
 Embolism or thrombus
 Arterial spasm
  Vasoconstriction
 Positioning
 Cardiopulmonary:
 Pulmonary embolism
 Low hemoglobin
 Myocardial ischemia
 Vasospasm
 Hypovolemia
 Cerebral:
 Increased intracranial pressure (ICP)
 Vasoconstriction
 Intracranial bleeding
 Cerebral edema
 Renal:
 Chemical irritants
 Hypovolemia
 Reduced arterial flow
 Hemolysis
 Gastrointestinal:
 Hypovolemia
 Obstruction
 Reduced arterial flow
Expected Outcome:
Patient maintains optimal tissue perfusion to vital organs, as evidenced by
strong peripheral pulses, normal ABGs, alert LOC, and absence of chest pain.

Ongoing Assessment

• Assess for signs of decreased tissue perfusion (see Defining

Characteristics for each category in this care plan).

• Assess for possible causative factors related to temporarily

impaired arterial blood flow. Early detection of cause facilitates
prompt, effective treatment.
 • Monitor international normalized ratio (INR) and prothrombin
time/partial thromboplastin time (PT/PTT) if anticoagulants are used
for treatment. Blood clotting studies are used to determine or
ensure that clotting factors remain within therapeutic levels.

• Monitor quality of all pulses. Assessment is needed for ongoing

comparisons; loss of peripheral pulses must be reported or
treated immediately.
Therapeutic Interventions

• Maintain optimal cardiac output. This ensures adequate

perfusion of vital organs. Support may be required to facilitate
peripheral circulation (e.g., elevation of affected limb,
antiembolism devices).

• Assist with diagnostic testing as indicated. Doppler flow studies

or angiograms may be required for accurate diagnosis.

• Anticipate need for possible embolectomy, heparinization,

vasodilator therapy, thrombolytic therapy, and fluid rescue. These
facilitate perfusion when obstruction to blood flow exists or
when perfusion has dropped to such a dangerous level that
ischemic damage would be inevitable without treatment.
Specific Interventions
Peripheral

• Keep cannulated extremity still. Use soft restraints or arm boards

as needed. Movement may cause trauma to artery.

• Do passive range-of-motion (ROM) exercises to unaffected

extremity every 2 to 4 hours. Exercise prevents venous stasis.

• Anticipate or continue anticoagulation as ordered. Therapy may

range from intravenous (IV) heparin, subcutaneous heparin,
and oral anticoagulants to antiplatelet drugs.

• Prepare for removal of arterial catheter as needed. Circulation is

potentially compromised with a cannula. It should be removed
as soon as therapeutically safe.
• If compartment syndrome is suspected, prepare for surgical
intervention (e.g., fasciotomy). The facial covering over muscles is
relatively unyielding. Blood flow to tissues can become
dangerously reduced as tissues swell in response to trauma
from the fracture.

• If cast causes altered tissue perfusion, anticipate that physician will

bivalve the cast or remove it. This restores perfusion in affected
extremity.

• Administer oxygen as needed. This saturates circulating

hemoglobin and increases the effectiveness of blood that is
reaching the ischemic tissues.

• Position properly. This promotes optimal lung ventilation and

perfusion. The patient will experience optimal lung expansion
in upright position.

• Report changes in ABGs (e.g., hypoxemia, metabolic acidosis,

hypercapnia). Titrate medications to treat acidosis; administer oxygen
as needed. This maintains maximal oxygenation and ion balance
and reduces systemic effects of poor perfusion.

• Anticipate and institute anticoagulation as prescribed. This

reduces the risk of thrombus.

• Institute continuous pulse oximetry and titrate oxygen

administered. This maintains adequate oxygen saturation of
arterial blood.
Cardiovascular

 Administer nitroglycerin (NTG) sublingually for complaints of

angina. This improves myocardial perfusion.

 Administer oxygen as ordered.

Cerebral

 Ensure proper functioning of intracranial pressure (ICP) catheter (if

present).
 • If ICP is increased, elevate head of bed 30 to 45 degrees. This
promotes venous outflow from brain and helps reduce
pressure.

• Avoid measures that may trigger increased ICP (e.g., straining,

strenuous coughing, positioning with neck in flexion, head
flat). Increased intracranial pressures will further reduce
cerebral blood flow.

• Administer anticonvulsants as needed. These reduce risk of

seizure, which may result from cerebral edema or ischemia.

• Reorient to environment as needed. Decreased cerebral blood

flow or cerebral edema may result in changes in the LOC.
Education/Continuity of Care

• Explain all procedures and equipment to the patient.

• Instruct the patient to inform the nurse immediately if symptoms of

decreased perfusion persist, increase or return (see Defining
Characteristics of this care plan).

• Provide information on normal tissue perfusion and possible causes

for impairment.
http://www1.us.elsevierhealth.com/MERLIN/Gulanick/Constructor/index.cfm?
plan=55

http://www1.us.elsevierhealth.com/Evolve/Ackley/NDH7e/Constructor/index.php