• HIV Infection and AIDS
• Diphtheria
• Encephalitis
• Hepatitis
• Herpes: Disseminated
• Measles
• Meningitis
• Mononucleosis
• Mumps
• Pertussis
• Shingles (Herpes Zoster)
• Tuberculosis
• Varicella (Chickenpox)
• Lice
• Scabies
• Myiasis
Major Topics
• Adrenal Crisis
• Diabetic Ketoacidosis
• Hyperglycemic Hyperosmolar Nonketotic Coma
• Hyperglycemia
• Myxedema Coma
• Thyroid Storm
HIV Infection and AIDS
Caused by a retrovirus
Viral symptoms start 2-6 weeks
Antibody seroconversion takes place within 45 days - 6 months
Asymptomatic period for months to years
• Replication, mutation, and destroying the immune system
HIV Infection and AIDS
• Persistent generalized lymphadenopathy occurs
• Constitutional disorders, neurological disorders, secondary infections, secondary cancers, and pneumonitis
HIV Infection and AIDS
All HIV infections will develop into AIDS
• Mean between exposure to HIV to AIDS-10 years
• AIDS to death
• Sooner the treatment, better long-term survival
HIV Infection and AIDS
Assessment
Subjective data
• History of present illness
Generalized lymphadenopathy, persistent
Fever for longer than 1 month
• Episodic spiking
• Persistent low-grade fever
Diarrhea for longer than 1 month
Weight loss
Anorexia
Night Sweats
HIV Infection and AIDS
Assessment
• Malaise or fatigue, arthralgias, myalgias
• Mild opportunistic infections
1.
Oral candidiasis
2.
Herpes Zoster
3.
Tinea
• Skin lesions, rashes
• Cough
• Broad range of neurological complaints, both focal and global, including dementia
HIV Infection and AIDS
Assessment
1.
Antiretroviral agents : zidovudine (AZT), zalcitabine (ddC), didanosine (ddI), stavudine (d4T), lamivudine (3TC), nevirapine, delavirdine
2.
Pneumocystis prophylaxis : trimethoprimsulfamethoxazole, pentamidine, dapsone
3.
Protease inhibitors: indinavir, saquinavir mesylate, nelfinavir, ritonavir
HIV Infection and AIDS
Assessment
Medical History
Blood transfusions, especially before 1985
Hemophilia
Occupational needle sticks or blood exposure
Sexually transmitted diseases (STD’s)
Tissue transplantation
Infant with HIV-positive mother
Sexual contact with IV drug user
Sexual contact with HIV-positive partner
Sexual practices including multiple partners, anal sex, oral-anal sex, or fisting
Recent TB exposure
HIV infection and AIDS
• Physical examination
Chronically ill appearance
Kaposi’s sarcoma skin lesions
Chest: crackles and wheezes
Dyspnea
Abnormal vital signs
Lymphadenopathy
Dementia
Wasting syndrome; signs of volume depletion
Withdrawn, irritable, apathetic, depressed
Slow, unsteady gait; weakness; poor coordination
HIV Infection and AIDS
• Diagnostic procedures
CXR
CBC
• Anemia
• Lymphopenia
• Thrombocytopenia
ABG’s
Electrolytes, liver function tests
HIV Infection and AIDS
Assessment
Determination of HIV antibodies (e.g., via enzyme-linked immunosorbent assay
[ELISA] and Western blot analysis)
decreased CD4 cell count
blood cultures
urinalysis
TB skin test (5 mm is positive in HIV infected person)
Diphtheria
Alteration in neurological functions
• Lethargy
• Withdrawal
• Confusion
• Cranial nerve neuropathies
Alteration in cardiac functions
• ST-and T-wave changes
• First-degree heart block
• Dyspnea, heart failure, circulatory collapse
Anxiety
Diphtheria
• Throat culture: specimen swabbed from beneath membrane or piece of membrane
• Notify lab that C. diphtheria is suspected: requires special media and handling
Diphtheria
Interventions
• Provide strict respiratory isolation
• Maintain airway, breathing, circulation
Monitor vital signs and pulse ox
Assemble emergency cricothyrotomy equipment at bedside
Administer O2 for dyspnea or cyanosis
• Establish IV catheter for administration of IV fluids
Diphtheria
Diphtheria antitoxin
• Equine serum
• Test for sensitivity
(intradermal or mucous membrane) before administration
• Often administered before diagnosis is confirmed because of virulence of disease
Diphtheria
• Antibiotic: EES or PCN G
• Antitussive
• Antipyretic
• Topical anesthetic agent
Minimize environmental stimuli
Instruct patient on importance of complete bed rest
Diphtheria
• Regular booster Q10years, combined with TD, after completion of initial series of 3 doses
• Identify close contacts
Culture and prophylactic Booster of TD in none within 5 years
Antibiotics
Active immunization for nonimmunized persons (series of 3 doses)
Encephalitis
Viral infection of the brain
Often coexists with meningitis and has broad range of S&S
Most cases in North America, caused by arboviruses, herpes simplex I, varicella-zoster, EB, and rabies
Transmission by animal bites, or seasonally form vectors (mosquitoes, ticks, and midges)
More common human viruses are airborne via droplet or lesion exudate
All age groups, with mortality from 5-10% from arboviruses and 100% for rabies
Encephalitis
Assessment
• Subjective
History of present illness
• Recent viral illness or herpes zoster
• Recent animal or tick bite
• Travel to endemic area, season of the year
• Fever
• Headache
Photophobia
Nausea, vomiting
Confusion, lethargy, coma
New psychiatric symptoms
Encephalitis
Assessment
• Subjective
Medical history
• Immune disorders
• Allergies
• Medications
Encephalitis
• Objective data
Physical exam
• Altered LOC
• Rash specific to cause
• Meningism
• Altered reflexes
• Focal neurological findings
• Abnormal movements
• Seizures
Encephalitis
• Diagnostic Procedures
Lumbar puncture, CT scan
CBC
Blood cultures
Serology
Encephalitis
Interventions
• Institute standard precautions and isolation until causative agent identified
• Monitor airway, breathing, circulation
• Monitor vital signs and pulse oximeter
• Administer O2
• Prepare to assist with intubation
• Insert large bore IV catheter, and administer isotonic solutions as ordered
• Administer medications as ordered
Encephalitis
• Administer antimicrobial/antiviral agents, steroids
• Monitor blood sugar and electrolytes
• Insert urinary catheter PRN
• Monitor I&O, cerebral edema, keep
HOB >30 degrees
• Institute seizure precautions
• Elevate HOB 30 degrees
Encephalitis
• Restrict IV fluids
• Keep body temperature normal
• Administer diuretics as ordered
• Explain procedures and disease to family/patient
• Allow patient/significant others to verbalize fears
• Prepare patient/family for admission to hospital
Hepatitis
Viral syndrome involving hepatic triad
(bile duct, hepatic venule, and arteriole, and central vein area.
Hep A-fecal-oral route, infectious for 2 weeks before and 1 week after jaundice
Hep B-(HBV)blood and sexual contact and consists of 3 antigens
• Hep B surface
Hepatitis
Hep B-(HBV) blood and sexual contact
3 antigens
• Hep B e antigens
• Dane particle- two part antigen: inner core
(hep B core antigen) and surface antigen (hep surface antigen)
Persistence of core antibody indicates chronic infection
Persistence of surface antibody indicates immunity to reinfection
Hep B surface antigen in the serum without symptoms is indicative of a carrier state
Hepatitis
Hep C identified by antihepatitis C virus antibody
50% of Hep C become chronic, and no immunity is developed
Hep C 90% of hepatitis cases transmitted by blood transfusion
Hepatitis
is an epidemic, enterically transmitted infection from shellfish and contaminated water
Hep D found with acute or chronic
HBV infection
Chronic infections result in cirrhosis and liver cancer
Hepatitis
Assessment
• History of present illness
Prodrome: preicteric phase, occurs 1 week before jaundice
• Low-grade fever
• Malaise: earliest, most common symptom
• Arthralgias
• Headache
• Pharyngitis
• Nausea, vomiting
Hepatitis
History of Illness cont’d
Rash, with type B usually
• May or may not progress to icteric phase
• Incubation:
A 15-45 days
B 30-180 days
C 15-150 days
• Duration:
A 4 weeks;
B AND C 8 weeks
Hepatitis
Icteric phase
• Disappearance of other symptoms
• Anorexia
• Abdominal pain
• Dark urine
• Pruritus
• Jaundice
Hepatitis cont’d
• Medical History
Immunizations
ETOH consumption
Allergies
Medications: all are significant
Blood transfusions, IV drug use, Hemophilia or dialysis
Chronic medical problems, travel, living in institution
Living in recent floods or natural disasters
Hepatitis
• Objective data
Physical exam
• Posterior cervical lymph node enlargement
• Enlarged, tender liver
• Splenomegaly in 20%
• Jaundice
• Vital signs: may have tachycardia, hypotension
• Fever
Hepatitis
Diagnostics
• Liver enzymes: SGOT & SGPT elevated
• Direct and indirect bilirubin levels: elevated
• Alkaline phosphatase : elevated
• Differential leukocyte count: leukopenia with lymphocytosis, atypical lymphocytes
• CBC, UA: elevated bilirubin, PT: elevated, ABD X-ray
• Antigen and/or antibody titers
Hepatitis
Interventions
• Provide increased calories
• Monitor for signs of dehydration, replacement with isotonic solution
• Record I&O
• Assess support systems of patients
• Hospitalize if unable to care for self or PT >15 seconds
Hepatitis
Initiate prophylaxis
• Type A
Immune serum globulin 80-90% effective if 7-14 days after exposure
Vaccine administered in two doses: given to high-risk population: foreign travel, endemic areas (e.g.
Alaska), military, immunocompromised or risk for HIV, chronic liver disease, hep C
• Type B: hepatitis B immune globulin plus vaccination, for exposure to serum, saliva, semen, vaginal secretions, breast milk
Hepatitis
Initiate prophylaxis
• Type B: vaccination with HBV vaccine inactivated
(Recombivax HB)
Vaccinate high-risk persons
• Health care and public safety workers, clients and staff at institutions
• Hemodialysis patients, recipients of clotting factors
• Household contacts and sexual partners of HBV carriers
• Adoptees from countries where HBV in endemic:
Pacific Islands and Asia
• IV Drug users, sexually active homosexual and bisexual men
• Sexually active men and women with multiple partners
• Inmates of long-term correctional facilities
Hepatitis
Vaccinate all infants (universally) regardless of hepatitis B surface antigen status of mother (administer first dose in newborn period, preferably before leaving hospital)
• Report to appropriate health departments
• Limit exposure of medical personnel to blood, secretions, and feces
Hepatitis
• Instruct patient/significant others
Strict hygiene, private bathroom if possible
Diet of small, frequent feedings low in fat, high in carbs, patient should avoid handling food to be consumed by others
S&S: bleeding, vomiting, increased pain
Take meds as prescribed
Avoid intake of alcohol
Take meds only if necessary
Avoid steroids: they delay long-term healing
Herpes: Disseminated
Herpes simplex virus (HSV) is a relatively benign disease when cutaneous
Can invade all body systems and lead to death
Primary viremia occurs from spill-over of the virus at the site of entry
During the second stage, HSV disappears from he blood but grows within cells of infected organs, which in turn causes seeding to other organ systems.
Dissemination occurs in susceptible persons: newborns, malnourished children, children with measles, people with skin disorders, such as burns, eczema, immunosuppression, and immunodeficiency, especially HIV
Herpes: Disseminated
HSV has a predilection for temporal lobe.
Encephalitis most common
• 70% mortality rate without treatment
• 50% with treatment residual neurological deficits
Latency period within sensory nerve resulting in mild or life-threatening infection years later
Herpes
History of present illness
• Onset: usually acute
After other illness
After outbreak of cutaneous infection
After any stressor
Herpes
• Subjective data
History of present illness
• Symptoms depend on organ system affected
Neurological system: headache, confusion, seizures, coma, olfactory hallucinations
Liver: ABD pain, vomiting
Lung: cough, fever
Esophagus: dysphagia, substantial pain, weight loss
Herpes
• HSV infection
• Chronic illness, cancer, HIV
• Medications: immunosuppressants
• Allergies
Herpes
• Physical exam
Fever
Other vital sign abnormalities depend on organ system involved
Focal neurological signs
• Anosmia (loss of smell)
• Aphasia
• Temporal lobe seizures
• Confusion, somnolence, coma
Respiratory
• crackles
Herpes
• Diagnostic Procedures
Viral cultures: blood and skin
Lumbar puncture: cerebrospinal fluid for culture
Biopsy of target organ, especially brain
Clotting studies for DIC
Liver Function
CBC
Herpes
Interventions
• Prepare to assist intubation
• O2 PRN
• Monitor
VS with PO
Neurological status
• Maintain airway, breathing, circulation
I&O
• Administer Antiviral meds
• FC PRN
• Establish IV of isotonic solution at rate to maintain blood pressure and fluid balance
• Protect from injury from seizures
• Explain procedures and illness to patient or significant others
• Practice standard precautions
Measles
Highly acute and contagious virus
Caused by rubeola virus, late winter and early spring
Airborne droplets, incubation 10-14 days
Contagious few days before and after onset of rash
Most recover, incidence of OM, diarrhea, pneumonia, and encephalitis
Measles
More serious in infants and in malnourished children, pregnancy with preterm delivery and spontaneous abortion
Most born <1957 are permanently immune
Vaccine (MMR) 12-15 months, active disease or two immunizations in childhood
Booster elementary school, all high school or college revaccinated unless active disease or two immunizations
Assessment
Measles
• Subjective data
History of present illness
• Exposure to measles
• Prodrome
Fever
Cough
Coryza (nasal mucosal inflammation)
Photophobia
Anorexia
Headache
Rarely seizures
Measles
Medical history
• Immunizations
• History of measles
• Current age: born before 1957
• Allergies
• Medications
Measles
Physical exam
• Fever
• Koplik’s spots on buccal mucosa
(bluish-gray specks on red base)
• Conjunctivitis
• Harsh cough
Measles
• Red, blotchy rash
Appears on third to seventh day
Maculopapular, then becomes confluent as progresses
Starts on face, then generalized to the extremities
Mild desquamation
Lasts 4-7 days
• Vital signs: normal, except fever
• Neurological system: may have altered
LOC, encephalitis
• Respiratory system: may have OM, pneumonia
Measles
Diagnostic procedures
• Viral cultures (expensive and difficult, so not usually done)
• Immunoglobulin M antibodies: measles specific
• CBC: leukopenia
• Other studies if seriously ill
Measles
Interventions
• Provide respiratory isolation
• Isolate patient/significant others from other people in waiting room
• Advise patient to avoid school, day care centers, and people outside immediate family until after contagious period
• Initiate immunization of high-risk contacts
Live vaccine if given within 72 hours of exposure (use monovalent vaccine if infants younger than 12 months; need reimmunization at 15 months with
MMR)
Immune globulin up to 6 days after exposure
Immunocompromised persons should receive immune globulin even if previously immunized
Measles
Encourage rest in darkened room
Administer acetaminophen for fever
Encourage parents to have children immunized at appropriate times
Instruct patient/parent about S&S of serious illness or complications
• Persistent fever or cough
• Change in mental status or seizures
• Difficulty in hearing
Meningitis
Bacterial or viral of the pia and arachnoid meniges
Late winter or early spring
Viral mild and short lived
Bacterial severe and life threatening
Streptococcus pneumoniae, Haemophilus influenzae (H. flu), and Neisseria meningitidis subgroups A, B, and C
H. Flu incidence decreased because of vaccination
Bacteria can enter the blood, basilar skull fracture, infected facial structures, and brain abscesses
Meningitis
Bacteria initially colonize in the nasopharynx
In bacterial disease, the subarachnoid space is filled with pus, which obstruct CSF, resulting in hydocephalus and increased ICP
Infants and elderly often do not exhibit classic signs of meningeal irritation and fever
Death most common within a few hours after diagnosis
Up to 33% of pediatric survivors left with some type of permanent neurological dysfunction
Any infant younger that 2 months with a fever, must be evaluated for meningitis
Meningitis
Assessment
• Subjective data
History of present illness
• Antecedent illness or exposure
• Onset: sudden
• Headache, especially occipital
• Fever and chills
• Anorexia or poor feeding
• Vomiting and diarrhea
Malaise, weakness
Neck and back pain
Restlessness, lethargy, altered mental status
Disinclination to be held: infants
Seizures
Recent basilar skull fracture
Meningitis
Medical history
• Medications
• Allergies
• Immunizations if child
• Chronic disease: liver or renal, DM, multiple myeloma, alcoholism, malnutrition
• Asplenic
• Recurrent sinusitis, pneumonia, OM, mastoiditis
Meningitis
Objective data
• Physical examination
High-pitched cry in infants
Hyperthermia >101 or hypothermia <96
Petechiae that do not blanch: 1-2 mm on trunk and lower portion of body, also mouth, palpebral and ocular conjunctiva
Purpura
Cyanosis, mottled skin, and pallor
Meningitis
Objective data
• Physical examination
• Vital signs
Tachycardia, hypotension, tachypnea
Bradycardia in neonates
• Meningeal irritation: persons older than 12 months, seen in about 50%
Contraction and pain of hamstring muscles occur after flexion and extension of leg: Kernig’s sign
Bending of neck produces flexion of knee and hip; passive flexion of lower limb on one side produces similar movement on other side:
Brudzinski’s sign
Nuccal rigidity
Meningitis
Infants with meningeal irritation cry when held and are more quiet when left in crib
Photophobia
Focal neurological signs, cranial nerve palsies, and generalized hyperreflexia
Altered mental status
• Confusion, delirium, decreased LOC
• Lethargy and confusion may be only signs in elderly
Bulging fontanelle
Irritability
Meningitis
Diagnostic procedures
• Blood glucose levels: infants younger than 6 months are prone to hypoglycemia
• Electrolyte levels: hyponatremia
• BUN and creatinine levels
• Serum osmolality
Low because of inappropriate vasopressin secretion
High because of dehydration
Meningitis
Diagnostic procedures
• CBC
Bacterial: high WBC
Viral: normal or low WBC
Meningococcal: WBC tends to be less that 10,000
• Blood cultures
• ABG’s if severely ill
• Clotting studies
• UA
• CXR and skull radiographs
Meningitis
Lumbar puncture: CSF
• Bacterial infection : cloudy appearance; elevated pressure;
WBC 200-20,000 with increased polymorphonuclear cells; glucose level decreased; protein level elevated; bacteria present on Gram’s stain
• Viral infection : clear appearance; WBC <500; normal pressure; glucose level normal; no bacteria present on Gram’s stain
Meningitis
Interventions
• Ensure that health care providers wear masks if infection with meningococcus is suspected
• Undress patient completely to check for petechiae
• O2 PRN
• Monitor VS
• Prepare to suction and assist with aggressive ventilatory support as needed
• Prepare to assist with LP
• Insert NG to prevent aspiration
Meningitis
Establish IV catheter, IO in necessary
Monitor IV fluids as related to I&O or excessive secretion of antidiuretic hormone
KCL replacement PRN, antiemtics PRN
Infuse antibiotics (usually ampicillin, aminoglycosides, cephalosporins)
Administer benzodiazepines, corticosteroids
Control fever
Reduce ICP
• Use hyperventilation with caution to avoid cerebral ischemia
• Elevate HOB 30 degrees
• Administer barbiturates and diuretics
Meningitis
Insert FC, monitor I&O
Monitor for signs of dehydration or fluid excess
Monitor mental status and neurological signs every
15 minutes to 1 hour, depending on patient’s stability
• May need to restrain confuse patient
• Protect seizing patient form physical harm
Explain procedures and need for ICU
Meningitis
Administer chemprophylaxis(rifampin, ceftriaxone) within 24 hours of disease identification to household contacts, day care center contacts, and health care providers if bacterial disease
• Side effects GI, lethargy, ataxia, chills, fever, and redorange urine, feces, sputum, tears, and sweat
• Soft contact lenses may be permanently stained with rifampin use
• Medication may need to be taken with food for GI intolerance, although it is best absorbed on empty stomach
• Birth control pills may not work
• Do not give to pregnant women
Meningitis
Educate parents to have infants immunized against H. Flu B beginning at 2 months
Mononucleosis
Acute viral illness with broad range of S&S lasting 2-3 weeks, very contagious
EBV transmitted in saliva
• About 50% of the population serovonverts to EBV before 5 years of age with sublclinical infection or mild illness
• Another wave of seroconversion in med adolescence
• Peak 15-24-years
Incubation 2-5 weeks
CMV is the other most frequent causative agent
Complications include: glomerulonephritis, autoimmune hemolytic anemia, pericarditis, hepatitis, guillain-Barre syndrome, meningitis, and pneumonia
Mononucleosis
Rarely death may occur from splenic rupture or airway obstruction as a result of tonsillar hypertrophy
• Subjective data
• History of present illness
Prodrome lasting 3-5 days: malaise, anorexia, nausea and vomiting, chills/diaphoresis, distaste for cigarettes, headache, myalgias
Mononucleosis
• History of present illness
Subsequent development of fever 100.4 to 104 lasting 10-14 days, sore throat,diarrhea, earache
• Medical history
Exposure to mononucleosis, usually not known
Allergies
Medications
Mononucleosis
Objective data
• Physical examination
May appear acutely ill
Red throat with exudate; tonsils may be hypertrophied
Tender lymphadenopathy, particularly posterior cervical
Petechiae on palate
Fine red macular rash 5% of adults: if given ampicillin,
90-100% of patients will experience rash
Abdominal tenderness with heptomegaly
Splenomegaly in 50% of patients
Mononucleosis
Diagnostic procedures
• Heterophile antibody titer (Monospot): positive by second week of illness; may remain negative in children younger than 5 years
• Throat culture to rule out group A streptococcus
• CBC: neutropenia, thrombocytopenia, lymphocytosis with atypical lymphs, leukocytosis
• Liver functions: may be abnormal
• CXR if pneumonia suspected
Mononucleosis
Interventions
• Isolation not necessary
Avoid kissing
No sharing eating or drinking utensils
• Activity as tolerated
Extra rest early in illness
Avoid heavy lifting and contact sports for at least 4 weeks if splenomegaly present
Mononucleosis
• Administer antipyretics, analgesics
(Avoid ASA)
• Administer corticosteroids therapy for severe Pharyngitis, evolving airway obstruction, chronic or disabling symptoms, or profound splenomegaly
Mononucleosis
• Warm salt water gargles for sore throat
• Encourage fluids to avoid dehydration
• Diet as tolerated
Liquids initially
Soft foods
• Do not donate blood for 6 months
Mononucleosis
Instruct patient about S&S of serious illness or complications
• Increased fever
• Cough, chest pain
• Progression of innless
• Difficulty breathing
• Signs of dehydration
• Increasing abdominal pain
Mumps
Acute, usually benign, viral infection caused by
Paramyxoviridae family
Swelling and tenderness of salivary glands and one or both parotid glands
Direct contact, droplet nuclei, or fomites
Incubation averages 16-18 days
Peak incidence is January to May
Most contagious just before swelling
More severe illness in the post pubertal age group; 20-
30% of adult men experience epididymoorchitis
Complications include viral meningitis, arthritis, arthralgias, and pancreatitis
Mumps
Assessment
• Subjective data
History of present illness
• Exposure to mumps
• Prodrome: fever (<104), anorexia, malaise, headache
• Earache and tenderness of ipsilateral parotid gland
• Citrus fruits or juices increase pain
• Fever, chills, headache, vomiting if meningitis
• Testicular pain if orchitis
• Abdominal pain if pancreatitis
Mumps
Subjective cont’d
Medical history
Childhood immunizations
Previous mumps
Allergies
Medications
Mumps
Objective data
• Physical examination
Swelling of gland, maximal over 2-3 days, with earlobe lifted up and out and mandible obscured by swelling
Trismus with difficulty in pronunciation and chewing
Testicle warm, swollen, tender
Scrotal redness
Mumps
Diagnostic procedures
• CBC: WBC and differential normal or mild leukopenia
• Serum amylase elevated for 2-3 weeks
Mumps
Interventions
• Provide respiratory isolation
• Advise to avoid school/work until swelling gone
• Administer analgesics
• Encourage rest until feeling better
• Encourage fluids, avoid citrus
• Warm or cold packs
• For orchitis
Bed rest
Scrotal elevation
Ice packs
Pain meds
Mumps
• Administer IV fluids for acutely ill patients
• Recommend immunization to family and health workers who have no mumps antibodies
Pertussis
Acute, widespread, highly contagious bacterial disease of the throat and bronchi
Gram-negative Coccobacillus Bordetella Pertussis
Airborne droplets
Most common children <4 years
Females higher incidence of morbidity and mortality
Partially immunized children have less severe illness
Adults have only minor respiratory symptoms and persistent cough, majority unrecognized
Pertussis
Vaccine immunity is <12 years, most adults are not protected
Incubation period 7-10 days but can vary 6-21
Peak incidence is during late summer and early fall
Pertussis bacteria invade the mucosa of URT
Complications include: pneumonia, pneumothorax, seizures, and encephalitis
Children also frequently experience laceration of the lingual fremulum and epistaxis
Pertussis
Assessment
• Subjective data
History of present illness
• Exposure to pertussis
• Three stages: last up to 2 weeks
Conjuctivitis and tearing
Fever/chills
Rhinorrhea, sneezing
Irritability
Fatigue
Dry nonproductive cough, often worse at night
Pertussis
Paroxysmal: lasts 2-4 weeks
• Severe cough with hypoxia, unremitting paroxysms, and clear, tenacious mucous; patient appears well between paroxysims of coughing; cough often triggered by eating and drinking
• Apnea can occur in rate cases
• Vomiting follows cough
• Anorexia
Convalescent: residual cough
Pertussis
Medical history
• Recent illness or infection
• Medications
• Allergies
• Immunization status
Pertussis
Objective data
• Physical exam
Paroxysmal explosive coughing ending in prolonged high-pitched crowing inspiration
Coryza
Clear, tenacious mucous in large amounts
Temperature >101
Restlessness
Crepitus from subcutaneous emphysema
Periobital/eyelid edema
Pertussis
• C&S testing of nasopharynx using calcium alginate dacron-tip swab
• Immunofluorescent antibody staining of nasopharyngeal specimens
• CBC with differential leukocyte count: lymphocytosis
Pertussis
Interventions
• Maintain respiratory isolation
• Monitor vital signs and respiratory status
• Be prepared to assist with intubation
• O2 PRN
• Isolate patients with active disease from school or work until they have taken antibiotics for 14 days
• Monitor for signs of dehydration or nutritional deficiency secondary to vomiting
Pertussis
Administer prescribed medication
• Antibiotic: EES
• Antitussive
• Analgesic
• Antipyretic
Position comfortably
Pertussis
Admit patients younger than 1 year: prepare for nasotracheal suctioning
Initiate immunization
• Educate parents about importance of complete immunization
• Household and other contacts <1year: prophylactic EED
• Household and close contacts ages 1-7 years who had less than four DTP vaccine doses or more that 3 years since:
EES for 14 days
DTP immunization
Pertussis
Review S&S that necessitate return to
ER
• Difficulty in breathing recurs or worsens
• Blue color of lips or skin
• Restlessness or sleeplessness develops
• Medicines are not tolerated
• Fluid intake decreases
Shingles (herpes zoster)
Acute localized infection cause by varicella-zoster virus (VZV)
During chickenpox, VZV travels from skin lesions to sensory nerve ganglia sets up latent infection
Postulated that when immunity to VZV wanes, the virus replicates
VZV moves down nerves, causing dermatomal pain and skin lesions
Lasts up to 3 weeks
Exact triggers unknown, old age and immunosuppression are risk factors
Shingles
20% of population
4% second exposure
Fluid from lesion is contagious, but likelihood of transmission is low
Susceptible exposed persons may develop varicella (chickenpox)
Complications: post herpetic neuralgia, debilitation pain syndrome lasts several months, blindness, disseminated disease, and occasionally death
Shingles
Assessment
• Subjective data
History of present illness
• Pain, itching, tingling, burning of involved dermatome precede rash by 3 to 5 days
• Rarely headache, malaise, fever
Medical history
• History of chickenpox, HIV infection, cancer, chronic steroid use
• Allergies
• Medications
Shingles
Objective data
• Physical examination
• Tenderness over involved dermatome
• Rash
Unilateral; does not cross midline
Usually thoracic or lumbar dermatome
Small fluid-filled vesicle on red base
May become hemorrhagic
New lesions occur for about 1 week
Shingles
• Fever (low grade if present)
• Visual acuity, if eye involved
Diagnostic procedures
• Viral culture
• Other studies if seriously ill
Shingles
Interventions
• Provide contact isolation
• Advise patient to avoid school/work until all lesions are crusted over
• Recommend immunizations of high-risk contacts
• Varicella-zoster immune globulin (VZIG)
Shingles
Administer medications as prescribed
• Analgesics
• Antihistamines
• Antivirals (acyclovir, famciclovir) will lessen disease severity and incidence of post herpetic neuralgia if administered within 72 hours of onset of rash
Shingles
To prevent infection of lesions, cut fingernails short
Topical baking soda paste or baths and calamine lotion may help
Ophthalmological consult if facial/eye involvement
Instruct patient about S&S of serious illness or complications
• Increased fever
• Cough
• Becoming more ill
• Signs of skin infection
Skin infestations: Lice
Three types of lice infest humans:
• Pediculus humanus var corporis (human louse)
2-4mm, grayish-white, flattened, wingless, and elongated with pointed heads
Overcrowding and poor sanitation
Skin infestations: Lice
Three types of lice infest humans:
• P. humanus var capitis (human head louse)
Wider and shorter, resemble a crab
Eggs (nits) laid by female
Affects all socioeconomic groups
• Phthirus pubis (pubic or crab louse)
Sexually or close body contact
Can be seen eyebrows, eyelashes, axillary hair, and back and chests
33% with lice have 2 nd STD
Lice
Can cause significant cutaneous disease
Lice serve as vectors for typhus, relapsing fever, and trench fever
Lice
Assessment
• Subjective data
History of present illness
• Itching infected areas
• Fever, malaise in severe infection
• Exposure to lice
• Recent sharing of clothing, beds, combs/brushes
• Concurrent STD’s
Medical history
• Previous infestations
• Allergies
• Medications
• Objective data
Lice
Lice
Physical exam
• Excoriation of scalp
• Secondary bacterial infection, especially of scalp
• Weeping and crusting of skin
• Lymphadenopathy
• Small, red macules, papules on trunk
• Small,gray to bluish macules measuring <1cm on trunk(maculae ceruleae) from anticoagulant injected into skin by biting louse
• Nits on hairs
• Thick, dry skin, brownish pigmentation on neck, shoulder, back form chronic infection
• Signs of concurrent STD’s
Lice
Lice
• Contact isolation
• Advise patient/parent to avoid school/work until one treatment completed
• Administer analgesics, antihistamines, antibiotics
Lice
• Use pediculicides
Pyrethrin liquid
Permethrin crème
• Treat sexual contacts
Administer medications for STD’s
Instruct patient/parent that itching may continue after treatment: do not re-treat without physician order
Lice
Instruct patient/parent to
• Remove nits
• Soak hair with equal parts warm vinegar and water
• If eyelashes or eyebrows, apply layer of petroleum jelly
• Soak combs and brushes in pediculicide for 1 hour
• Launder clothing/bedding in hot water; dry in hot drier if possible, discard clothing and linen if practical
Lice
Lice
• Iron seams of clothing
• Put socks over hands of small children at bedtime
• Cut fingernails short
• Put hats, coats, other non-launderable item away for at lest 72 hours
• Avoid hat sharing, combs, brushes
Skin infestations: Scabies
Highly contagious by the itch mite
Sarcoptes scabiei var hominis
Eggs are laid in burrows several millimeter in length
Not a vector for other infections
Transmitted by intimate personal or sexual contact; or by casual contact
Always consider when patient complains of rash with intense itching
Scabies
• Subjective data
History of current illness
• Intense itching, worse at night
• Rash
• Previous treatment for current problem
• Exposure to scabies
Medical history
Previous infestations
Allergies
medications
Scabies
• Physical exam
Rash
• Red papules, excoriations, and occasionally vesicles
• More common in interdigit web spaces, wrists, anterior axillary folds, periumbilical skin, pelvic girdle, penis, ankles
• For infants and small children, soles, palms, face, neck, and scalp are often involved
• Patient scratching
• Signs of infection of lesions
Scabies
Interventions
• Contact isolation
• Advise patient/parent to avoid school/work until one treatment completed
• Administer analgesics, antihistamines, antibiotics
• Use pediculicides
Pyrethrin liquid
Permethrin crème
Scabies
Instruct patient/parent
• Instruct patient/parent that itching may continue after treatment: do not re-treat without physician order
• Launder clothing/bedding in hot water; dry in hot drier if possible, discard clothing and linen if practical
• Put socks over hands of small children at bedtime
• Cut fingernails short
• Put hats, coats, other non-launderable item away for at least 72 hours
Skin infestations: myiasis
Invasion of living, necrotic, or dead tissue by fly larvae (maggots)
Do not carry infectious agents, but can cause significant disease of the tissues
Skin infestations: myiasis
Assessment
• Subjective data
History of present illness
• Skin lesions or wound
Social History
Living conditions
• Ability to care for self
• Substance abuse
• Previous myiasis
• Medications
• Allergies
Myiasis
Objective data
• Physical examination
Skin wound or lesion
Boil-like lesion
“creeping eruption” of open wounds
Poor hygiene: may see maggots in skin folds or on intact skin surface
Myiasis
• Contact isolation
• Advise patient/parent to avoid school/work until treatment completed
• Administer analgesics and antibiotics
• Prepare to assist with surgical debridement
Myiasis
• Apply petroleum jelly to cutaneous boils
• Instruct patient about prevention
Eradicate flies
Keep open wounds properly dressed
Stay indoors, away from fly-infested areas
• Referrals to Social Services or
Substance Abuse if needed
Tuberculosis
Mycobacterium tuberculosis, acid-fast bacillus (AFB)
Not highly contagious, requires close, frequent exposure for transmission
Droplet nuclei, which can remain in still air for days
Susceptibility of host usually determines whether infection occurs
TB occurs when symptoms occur and is infectious
2-10 weeks after infection, develop immunological response, allows healing and +PPD
Tuberculosis
Greatest risk of disease in the first 2 years after infection
Lung primary site
15% Extrapulmonary
• Kidney, Lymphatic, Pleura, Bones, Joints, and blood
(disseminated or miliary)
Diagnosed by one of two criteria:
• Culture of bacteria
• + PPD or S&S of TB, unsteady CXR
Noncompliance of medication regimen
Tuberculosis
• Subjective data
History of present illness
• Exposure to TB
• Productive prolonged cough
Longer than 2 weeks
Becoming progressively worse
Tuberculosis
History of present illness
• Fever and chills, night sweats
• Easy fatigability and malaise
• Anorexia, weight loss
• Hemoptysis
• Recent +TB skin test
• Foreign born or travel to high-prevalence country: Vietnam, Philippines, Mexico, Haiti,
China, Korea
Tuberculosis
History of present illness
• Resident or staff of nursing home, prison, or homeless shelter
• Alcoholic or other substance abuser
• Racial/ethnic minority:
African-American, Hispanic,
Alaska native,
American Indian
Tuberculosis
Medical History
• DM
• Malignancy
• CRF
• Immunosuppression
• HIV and AIDS
• Medications, especially prolonged steroid therapy
• Allergies
Tuberculosis
Objective data
• Physical exam
• Healthy or ill appearance
• Chest: decreased breath sounds
• Fever
• Signs of underlying disease
Tuberculosis
Diagnostic Procedures
• PPD: induration 5mm or
> +if HIV, 10mm + all others
• CXR: infiltrate, especially of upper lobes
• Sputum for AFB: 3 successive earlymorning
• LFT: obtain before starting INH
Tuberculosis
Interventions
• Decrease transmission of disease
Isolate coughing patient, preferably in negative pressure
Teach to cover nose and mouth
Educate to dispose of tissue and wash hands
Isolate at home first 2 weeks of therapy; considered infectious until
• 14 days of directly observed therapy
• Decrease cough and afebrile
• Three consecutive negative AFB smears
Tuberculosis
Surgical masks are helpful for patient; not effective for health care staff or family
Ventilate living quarters with fresh air: 20 times every day
Unnecessary to dispose of clothes, to wear caps, gowns, gloves
• Encourage patient/significant other for reading of TB skin test, compliance with medication regimen
• Reportable disease
Tuberculosis
Administer and educate about meds
• All patients with active disease should have directly observed therapy
• Preventive therapy for 6 months
HIV with PPD +5> :treat 12 months
Household members and close contacts of newly diagnosed patient
Recent TB converter
IV drug users known to be HIV- with PPD induration of 10mm>
Tuberculosis
• Medications: preventative and therapeutic 4drug regimen
Isoniazid
Pyridoxine: prevents peripheral neuropathy from isoniazid
Rifampin: discolors
Pyrazinamide
Ethambutol
Encourage HIV testing
Provide Social Service in needed
Varicella (chickenpox)
Highly contagious caused by VZV
Direct contact, droplet, or aerosol from skin lesion fluid
Incubation 14-16 days
Contagious period start 1-2 days before rash and ends when all lesions are crusted
90% cases children <3
Varicella (chickenpox)
Adolescents, adults, and immunocompromised at risk for severe disease
<5% of cases >20 years, but 55% of deaths
Complications
• Bacterial infection, pneumonia, DIC, renal failure, and encephalitis
• 31% mortality to neonates born to infected mothers
Chickenpox- Assessment
Subjective data
• History of present illness
Exposure to chickenpox
Prodrome: 48 hours before rash: fever, malaise, headache, rash often with itching
• Medical history
Immunizations
Pregnant or trying to become pregnant
HIV, cancer, or other immunocompromised state
Allergies
Medications
Chickenpox
Objective data
• Physical exam
• Rash, typically 250-500 lesions
Starts on trunk as faint, red macules
Becomes teardrop vesicles on a red base, which dry and crust over
New crops appear over several days
Palms and soles are spared
Vesicles may occur in mucous membranes, rupture, and become shallow ulcers
Chickenpox
Objective data
• Fever, low grade
• Skin excoriations form scratching
• Signs of lesion infection: red, swollen, tender
• Altered mental status
• Dehydration
• Cough
Chickenpox
• Diagnostic procedures
Generally none
Chickenpox
Interventions
• Provided respiratory and contact isolation
• Isolate patient/significant others from waiting room
• Advise to avoid school/work until all lesions are crusted
Chickenpox
Interventions
• Recommend immunization of high-risk contacts
VZIG
• Post exposure prophylaxis
• Immunocompromised (HIV, AIDS, cancer, steroid therapy)
• Effective up to 96 hours after exposure
• Susceptible health care workers should be vaccinated
Chickenpox
Administer medications
• Acetaminophen
• Never use ASA (risk of Reye’s syndrome)
• Antihistamines
• Antivirals to older children will lesson the severity
To prevent infection of lesions
• Suggest putting socks over small children’s hands at bedtime to decrease scratching and excoriation
Chickenpox
• Cut fingernails short
• Topical backing soda paste or baths and calamine lotion
• Encourage parents to have children immunized
Chickenpox
Instruct patient/parent about S&S or serious illness
• Increased fever
• Cough
• Becoming more ill
• Signs of skin infection
Adrenal Crisis
Addison’s Disease (adrenal insufficiency)
Adrenal cortex ceases to produce glucocorticoid and mineralocorticoid hormones
Acute stressors, infection, hemorrhage, trauma, surgery, burns, pregnancy, or abrupt cessation for
Addison’s disease
Life threatening because hormones are necessary for the maintenance of blood volume, BP, and glucose homeostasis
Adrenal Crisis
Suspect with patients who have septicemia with unexplained deterioration, major illness who have abdominal, flank, or chest pain, with dehydration, fever, hypotension, or shock, and adrenal hemorrhage
Death because of circulatory collapse and hyperkalemiainduced dysrhythmia
Adrenal Crisis- Assessment
• History of present illness
Rapid worsening of symptoms of adrenal insufficiency
Fever
Nonspecific abdominal pain; may simulate acute abdomen
N&V
Adrenal Crisis- Assessment
Medical history
• Primary adrenal insufficiency
• Hyperpigmentation of skin
• Weakness, fatigue, lethargy
• Anorexia and weight loss
• Nausea, vomiting, diarrhea
• Salt craving
• Postural hypotension
• Allergies
• Medications
Adrenal Crisis
Physical examination
• Appears acutely ill
• Signs of shock as a result of dehydration
Hypotension, but may have warm extremities
Tachycardia
Tachypnea
Orthostatic hypotension
Adrenal Crisis
• Fever
• Altered mental status, confusion
• Hyperpigmentation of skin
• Very soft heart sounds
Adrenal Crisis
Diagnostic procedures
• CBC: anemia of chronic disease
• Electrolyte levels
Hyponatremia
Hyperkalemia
• Blood glucose level: hypoglycemia
• BUN: elevated (azotemia secondary to dehydration)
• UA
Adrenal Crisis
UA
Blood cultures
Plasma cortisol level
ECG
• Low voltage
• Flat or inverted T wave
• Prolonged QT, QRS, or PR intervals
• CXR
• CT of abdomen: if diagnosis not clear
Adrenal Crisis
Interventions
• O2, IV, monitor
• VS, with Orthostatic VS
• I&O
• Weight
• Monitor signs of adequate tissue perfusion: capillary refill and skin temperature and moisture
Adrenal Crisis
• Medications
Dexamethasone
Hydrocortisone
Corticotropin
Glucose
Vasopressors
• Monitor electrolytes
• Monitor cardiac function
• Prepare for admission
• Instruct about disease process
Diabetic Ketoacidosis
Result of insulin deficiency
Typically Insulin-dependent
Hyperglycemia promotes osmotic diuresis with dehydration, hyperosmolality, and electrolyte depletion
Free fatty acids are converted to ketones bodies, which release hydrogen ions, thereby contributing to metabolic ketoacidosis
Diabetic Ketoacidosis
Infection and stressful events are usual precipitation factors, along with omission of insulin and new-onset diabetes
Goal is a gradual return to normal metabolic balance
Complications of therapy: cerebral edema, hypoglycemia, and electrolyte imbalance may contribute to death
Diabetic Ketoacidosis-
Assessment
Subjective data
• History of present illness
Onset: gradual, 24 hours to 2 weeks
Preceding bacterial or viral illness, current infectious process, or significant stress
N&V
Abdominal pain, usually generalized
Fever
Polyuria, polydipsia, polyphagia
Lethargy, weakness, and fatigue
Decreasing LOC and altered mental status
Weight loss
Diabetic Ketoacidosis
Medical history
• Administration of insulin or oral hypoglycemic agents
• Discontinuance or decreased dose
• Other medications
• Allergies
• Previous similar episodes
Diabetic Ketoacidosis
Objective data
• Physical examination
Tachycardia
Orthostatic or frank hypotension
Kussmaul’s respirations if pH <7.2
Dry, hyperthermic, flushed skin, poor turgor, dry mucous membranes
Acetone breath odor
Confusion, coma, and decreased mental status
Diabetic Ketoacidosis
Diagnostic procedures
• Serum glucose level: >300
• Electrolyte levels
NA, CL, and HCO3: decreased
K: normal or elevated initially; falls rapidly during treatment
Serum phosphate: elevated 6-7 as a result of insulin deficiency and prerenal azotemia; total body phosphate depletion as a result of osmotic diuresis
Diabetic Ketoacidosis
Diagnostic procedures
• Serum osmolality: >310
• Serum acetone level: elevated
• BUN and creatinine levels: normal unless advanced renal disease or severe dehydration is present
• ABG
Normal PaO2
Metabolic acidosis and anion gap acidosis: pH<7.3;
HCO3<15
Respiratory alkalosis
Diabetic Ketoacidosis
UA: increase glucose and ketone levels
CXR
ECG
CBC: WBC >25,000 if infection present
Cultures as indicated
Diabetic Ketoacidosis
Interventions
• Establish two IV’s, one for NS
• O2, airway, breathing, circulation
• Administer regular insulin as prescribed
Glucostabilizer Program
Diabetic Ketoacidosis
Interventions
• Administer HCO3 as prescribed: if pH
<7.0
• K: added to IV if < 5.5
• Add Dextrose when blood glucose <250
• Administer phosphate (usually several hours into treatment)
Diabetic Ketoacidosis
Administer antibiotic or antiemetics as ordered
Insert urinary catheter; NG if decrease LOC
VS every 15 to 60 until stable
Monitor glucose every hour and K every 2 hours
I&O
Cardiac monitor until stable, Neuro checks
(cerebral edema from too-rapid resolution of acidosis and hypoglycemia)
Diabetic Ketoacidosis
May need to restrain if confused
Review preventive fluid therapy
• Must keep self hydrated, during any illness, no matter how minor
• If unable to retain fluids, contact physician immediately
Teach to identify and manage symptoms of hypoglycemia or hyperglycemia
Hyperglycemic Hyperosmolar
Nonketotic coma
Type II, non-insulin-dependent
Profound dehydration because of hyperglycemia and resultant osmotic diuresis
Unable to drink
Ketoacidosis does not develop because there is enough endogenous insulin present to inhibit ketogenisis
Precipitated by infection, stroke, or sepsis
Hyperglycemic Hyperosmolar
Nonketotic coma
Initial presentation with new-onset type II DM
Dehydration predisposes to widespread thrombosis and DIC
Mortality rate is high despite aggressive therapy, probably because patient is usually elderly with impaired renal, cerebral, or cardiac function
Illness rarely occurs in infants and children
DKA
Serum Glucose:
HIGH
pH: <7.3
HCO3: <15 mEq/L
Serum Ketones: +
Ketonuria: +
Osmolarity: varies
Serum Insulin: decreased vs. HHNK
Serum Glucose:
VERY HIGH pH: >7.3
HCO3: >20 mEq/L
Serum Ketones: -
Ketonuria: -
Osmolarity: High
Serum Insulin: can be normal
NKH- Assessment
Subjective data
• History of present illness
Insidious onset from days to weeks
Recent illness or infection
Thirst
Reduced fluid intake
Polyuria or oliguria
• Medical history
Non-insulin-dependent diabetes
Elderly patient with undiagnosed diabetes
Medications: oral hypoglycemic agents, diuretics
Allergies
Objective data
• Physical examination
Hypotension and Tachycardia
Normal respirations
Confusion and altered mental status are most prominent physical findings; may be comatose
Dry skin and mucous membranes: dehydration
May have fever
Seizures
Hemiparesis/hemisensory deficits
HHNK
• Serum glucose level: >800mg/dl, often
>1000
• Serum osmolality:: >350mOsm/kg
• Hypernatremia resulting from dehydration
• K: normal to high initially; hypokalemia develops with insulin therapy
• BUN and creatinine: elevated as a result of prerenal azotemia
HHNK
Diagnostic procedures
• ABG’s
Normal PaO2
Mild metabolic acidosis
Serum ketone level: normal or slightly elevated
UA: elevated glucose level
CXR
ECG
Cultures of blood, urine, sputum if infection source not obvious
Creatine kinase (CK) elevated as a result of rhabdomyolysis
HHNK
• O2, airway, breathing, circulation
• Assist with intubation if PaO2 .70
• IV for hydration
Adults: NS at 500-1000ml/hr until blood pressure stabilizes
Child: NS (20 ml/kg bolus if hypotensive) to prevent cerebral edema from too-rapid correction of hyperosmolality
NKH
• K+ as needed
• Low dose heparin
• Add dextrose when glucose <300
• May need to restrain confused patient
• Continually reassess neurological status, and monitor for signs of cerebral edema and seizures
• I&O, FC
• Monitor for signs of fluid overload (major problem in elderly) or dehydration; assess breath sounds as indicated for pulmonary edema
• Discuss disease process
Hypoglycemia
Glucose <50
• most common endocrine emergency
<35 mg/dL, the brain in unable to extract O2 adequately, resulting in hypoxia and coma
Very young and very old are more susceptible
Mainly diabetes and alcohol ingestion, lack of glucose causes permanent brain dysfunction, any person with an altered LOC should be considered to have hypoglycemia until proven otherwise
Hypoglycemia- Assessment
History of present illness
• Rapid onset
• No recent food intake
• Alcohol ingestion within 36 hours followed by fasting
• Hunger, nausea
• Weakness, dizziness
• Lethargy
• Shakiness
• Anxiety
• Headache
• Altered mental status
Hypoglycemia
Medical history
• Diabetes
• Insulin: increased dosage (easily reversed)
• Oral hypoglycemic agents: long half-life
(difficult to reverse)
• Adrenal insufficiency
• Liver disease
• Propranolol, salicylates, sedatives
• Increase in physical exercise
Hypoglycemia
Physical exam
• Cool, diaphoretic skin, pale, dilated pupils
• Confusion, hypothermia
• Shallow respirations but normal rate
• Normal BP and pulse
• Combative behavior or coma, seizures
• Hemiplegia or other signs of stroke
Hypoglycemia
Diagnostic procedures
• Blood glucose level: <50
• Electrolyte levels: normal
• UA: normal
• ABG’s: normal pH
• Serum ETOH
Hypoglycemia
Interventions
• O2, VS, maintain airway, breathing, circulation
• Assist with intubation if PaO2 <70
• determine blood glucose level
• Administer thiamine IM or IV if malnourished
• Oral glucose if gag present
• D5w if unresponsive
• Give IV D50; if no response repeat; D25 if
<2yrs
• Give Glucagon IM or SC
Hypoglycemia
Interventions
• Monitor mental status continually
• May need to restrain combative patient
• Educate patient and significant others
Reinforce need to eat regularly
Carry quick glucose foods
Decrease insulin dosage if exercising
Avoid alcohol consumption while fasting, alcoholic need to eat when bingeing
Myxedema coma
Severe form of hypothyroidism
Marked impairment of CNS and cardiovascular decompensation
Recognition of this illness is hampered by its insidious onset and rarity
Winter, elderly women with HX of hypothyroidism
Precipitating factors include: serious infection
(pneumonia and UTI), sedative or tranquilizer use, stroke, exposure to cold environment, and termination or thyroid hormone replacement
Death is common, but can survive if prompt adequate care
Myxedema coma
History of present illness
• Recent illness
• Progressive decline in intellectual status
• Apathy, self-neglect
• Emotional labiality
• Anorexia
• Recent weight gain
Medical history
• Hypothyroidism or thyroid surgery
• Allergies
• Medications: thyroid replacement hormone, recent use of tranquilizers and sedatives
Myxedema coma
Objective data
• Physical exam
Decreased mental status
Depressed mental acuteness
Confusion or psychosis
Pale, waxy, edematous face with periorbital edema
Dry, cold, pale skin
Myxedema coma
Objective data
• Physical exam
Non-pitting extremity edema
Thin eyebrows
Deep, coarse voice
Scar form prior thyroidectomy
Vital Signs
• Hypothermia, usually above 95 F
• Bradycardia with distant heart sounds
• Hypoventilation, Hypotension
Myxedema coma
Diagnostic procedures
• Electrolytes: hyponatremia
• ABG’s: hypoxia and hypercarbia
• Thyroid studies: low thyroxine (T4), elevated thyrotropin (thyroid stimulating hormone [TSH])
Myxedema coma
ECG
• Low voltage
• Sinus bradycardia
• Prolonged QT interval
• CBC: anemia and decreased WBC
• BUN and creatinine: elevated
• Blood sugar: variable hypoglycemia
• CXR
• UA
• Obtain pretreatment plasma cortisol level
Myxedema coma
• Monitor airway, breathing, circulation, and other vital signs
• O2 as ordered
• IV, IV fluids
Hypertonic saline
Crystalloids
Whole blood
Myxedema coma
Interventions
• Meds as ordered
IV thyroid hormone
Glucocorticoid
Vasoconstrictors
• Rewarm patient
Use passive rewarming with blankets and increased room temperature
Avoid rapid rewarming
Be prepared for seizures
Thyroid storm
Extreme and rare form of thyrotoxicosis
High mortality
Untreated or inadequately treated hyperthyroidism, who experiences surgery, infection, trauma, or emotional upset; thyroid surgery; radioactive iodine administration
Cardiac decompensation with CHF (terminal event), CNS dysfunction, GI disorders
Life-threatening emergency
Thyroid Storm- Assessment
History of present illness
• Fever
• N&V&D
• Abdominal pain
• Worsening of thyrotoxicosis symptoms
• Anxiety
• Restlessness, nervousness, irritability
• Generalized weakness
• Possible coma
• Precipitation event or intercurrent illness
Thyroid storm
Medical history
• Thyrotoxicosis
• Thyroid disease
• Easy fatigability
• Weight loss
• Sweating
• Body heat loss and heat intolerance
Thyroid storm
Objective data
• Physical exam
Fever: temp may exceed 104
Tachycardia (120-200), systolic hypertension
Chest: crackles
Thyroid storm
• Warm, moist, velvety skin; becomes dry as dehydration develops
• Spider angiomas
• Tremulousness
• Delirium, agitation, confusion, coma
• Thin silky hair
• Enlarged thyroid gland with thrill or bruit
Thyroid storm
• Eye signs
Lid lag
Stare
Exophthalmos
Periorbital edema
• Hepatic tenderness or jaundice
Thyroid storm
Diagnostic procedures
• Cardiac monitoring/ECG: sinus tachycardia wand atrial fibrillation/flutter
• Thyroid function studies
T4: elevated
Triiodothyronine (T3): elevated resin uptake
TSH: decreased
• Serum cholesterol level: decreased
Thyroid storm
Diagnostic procedures
• Electrolyte levels
• Serum glucose increased
• CBC: increased WBC with left shift
• BUN or creatinine level
• Hepatic studies: increased liver enzymes
• UA
• Cultures and radiographs and indicated
Thyroid storm
Interventions
• O2, airway, breathing, circulation, VS
• IV of D5 and isotonic solution
• Cardiac monitoring
Meds as ordered
• Vasopressors
• Antipyretic
• D50
• Propylthiouracil every 8 hours
• Glucocorticoids, hydrocortisone
• Iodine: lugol’s solution, potassium iodide
• Digitalis, propranolol
• Antibiotics
• Vitamins and thiamine
• Sedatives
Thyroid storm
• Use cooling blanket, cold packs
• Prepare patient/significant others for patient’s admission
• Explain procedures to patient/significant others