MORTALITY REPORT

Case presentation

Discussion

Topic of interest

PATIENT DETAILS

Referred from casualty with three days history of sore throat

Difficulty in swallowing

Febrile episodes controlled by paracetamol

Hypertensive on treatment

No other history of note

54 YEARS MALE PATIENT

EXAMINATIONPatient comfortable in room air, afebrile to touch. No stridor. Voice sounds muffled but patient reports it has not changed

Points to submandibular region bilaterally as area of tenderness

Oral Exam: Hyperaemic oropharynx

No obvious infection in tonsillar crypts

No masses in the oropharynx

Ears: Normal clinical findings

Nose: congested mucosa, turbinates hyperaemic, no masses no discharge

Differentials:

Acute pharyngitis

Viral tonsillitis

Further examination

Epiglottis swollen with inward curling of lateral borders

Arytenoids hyperaemic

Vallecula and lateral pharyngeal wall hyperaemic

Vocal cords partially seen beyond the swollen epiglottis, appear normal and mobile

Flexible scope examination of larynx Diagnosis:

Acute Epiglottis

Management on admission @15H20

Patient convinced to be admitted for airway monitoring

Decadron 8mg stat prescribed

Ivi ceftriaxone 1g ivi 12 hrly

Decadron 8mg ivi daily

Paracetamol 1g orally for analgesics

Adrenaline:saline nebs 4 hrly or PRN

Ivi line inserted.

Bloods fbc, cusp taken

Soft tissue view of neck requested.

Special instructions for nursing staff:

Monitor patient and vitals 2 hourly

Monitor airway and any abnormal breathing

pattern and inform doctor if any noticed

PATIENT STATUS 6H15 pm patient certified deadSister in ward reported that patient got up to go to toilet and she noticed that patient was not “ok”

She called for assistance when patient collapsed

Code blue – unfortunately no response from any staff

Dr Gardiner informed, he informed me, when I got to hospital patient ready for transport to mortuary.

Resusc not attempted as there was no pulse, no pupillary reflexes, no attempts at respiration, patient was cold to touch.

DISCUSSION FORUM

Why did the patient die……

What was the cause of death???

EPIGLOTITIS

• Epiglottitis is inflammation of the epiglottis and adjacent supraglottic structures.

• Without treatment, epiglottitis can progress to life-threatening airway obstruction

Definition:

RELEVANT ANATOMY

PATHOGENISIS

Infectious epiglottitis is a cellulitis of the epiglottis, aryepiglottic folds and other adjacent tissues

It results from bacteraemia and or direct invasion of the epithelial layer by the pathogenic organism

The posterior nasopharynx is the primary source of pathogens in epiglottitis…

PATHPHYSIOLOGY Swelling of the epiglottis results from edema and accumulation of inflammatory cells in the potential space between squamous epithelial layer and epiglottic cartilage

Lingual surface of epiglottis and periepiglottic tissues have abundant networks of lymphatic and blood vessels that facilitate spread of infection and subsequent inflammatory response

Once infection begins, swelling rapidly progresses to involve the entire supraglottis including aryepiglottic folds and arytenoids

Subglottic not affected as swelling is halted by the true vocal cords

Supraglottic swelling reduces calibre of the upper airway, causing turbulent airflow during inspiration , further airflow obstruction may be due to posterior and inferior curling of the epiglottis which acts as ball valve, causing stridor and facilitating aspiration of oropharyngeal secretions

ETIOLOGY May be caused by number of bacterial, viral and fungal pathogens

CHILDREN: Haemophilus influenza

ADULTS: broad range of bacteria, viruses, combined bacterial-viral infections as well as fungi

In most adult cases blood and throat cultures are negative

Among cases in which pathogen is identified Hib is most common accounting for 3 – 14 % of all cases

IMMUNOCOMPROMISED: pseudomonas aeruginosa and candida species, single case reported in adult receiving steroids and azathroprine for chron’s disease

NONINFECTIOUS CAUSES: Traumatic causes include thermal injury, foreign body ingestion and caustic ingestion.

May rarely occur as manifestation of graft versus host disease etc

EPIDEMIOLOGY

Hib vaccine changed the epidemiology of the disease

Decreased average annual incidence in children. In USA annual rate prior to availability of Hib vaccine was 5/100000 in less than 5 years, currently immunized children rates are between 0.6 to 0.8/100000 as herd immunity improves with time the incidence is expected to lower

Incidence in adult 0.6 to 1.9 /100000 in Iceland and Denmark studies similar results in USA

Statistics similar in most developing countries with Hib vaccination programme.

EPIDEMIOLOGY

Increased age of children with Epiglottitis

Median age of children prior to vaccine was 3 years, post vaccination age has now increased to 6 to 12 years of age

Epiglottitis historically is somewhat more prevalent in boys (58%)

RISK FACTORS

In children – complete or lack of immunization for Hib and Immunosupression

In adults epiglottitis has been associate with number of comorbid conditions: HPT, DM, Substance abuse and Immune deficiency

Suspected Epiglottitis is a medical emergency….. Prompt recognition and treatment is critical

CLINICAL PRESENTATIONS Clinical feature of epiglottitis differ with age severity and etiology

Young children present with respiratory distress, anxiety and the characteristic “tripod” or “sniffing” posture in which they assume a sitting position with trunk leaning forward, heck hyperextended and chin thrust forward in an effort to maximize the diameter of obstructed airway

They may be reluctant to lie down

Drooling is often present

Older children, and adults may present with a severe sore throat but relatively normal oropharyngeal examination

CLINICAL PRESENTATION Abrupt onset and rapid progression of dysphagia, drooling and distress ( hallmark of epiglottitis)

Sudden onset of high fever between 38.8 to 40 degrees celcius is common together with severe sore throat, odynophagia and drooling

Children often appear “toxic”

Older children can describe a “choking sensation” distressed during inspiration, are often anxious and irritable. Speech is often muffled

Stridor is frequently present

Quality of voice is still normal

CLINCAL FEATURES ADULTS Sore throat or odynophagia (90 – 100%)

Fever greater than 37.5 degree celcius (26 – 90%)

Muffled voice (50 – 80%)

Drooling (15 – 65%)

Stridor or respiratory compromise (approx. 33%)

Hoarseness (20 – 40%)

EXAMINATION

Visualization of epiglottis is an accepted standard for clinical diagnosis

Radiographs are used to make diagnosis in patients with a mild disease, who then may be admitted for ivi antibiotics and close airway monitoring

The approach to diagnosis epiglottitis including flexible laryngoscopy, depend on patient’s age, degree of illness and clinician’s suspicion for epiglottitis

EXTRA EPIGLOTTIC FOCI OF INFECTION Patients should be examined for extra epiglottic foci of infection Pneumonia, cervical adenitis, cellulitis, septic arthritis, or

meningitis)

If pathogen that frequently causes invasive diseases at other site is a possibility (eg. S pneumonia, Haemophilus influenza b)

LAB – Laboratory studies should not be performed in patients in whom epiglottitis is strongly suspected until the airway is secured Agitation caused by pain may worsen resp distress LAB evaluation should include FBC, blood culture and epiglottal

culture in intubated patients

RADIOGRAPHIC FEATURES

CAUSATIVE ORGANISM

Review of 407 cases of epiglottitis from a single state over an 18 year period suggests that clinical features vary depending upon whether or not Hib is the causative pathogen

Mayo-Smith MF, Spinale JW, Donskey CJ, et al. Acute epiglottitis. An 18-year experience in Rhode Island. Chest 1995; 108:1640.

Hib epiglottitis is associated with ‘classic” features , more common in young children and is rapidly progressive, involves epiglottis more than the surrounding structures and has a high risk of airway obstruction

Non Hib epiglottitis is more common in adults and generally has a slower onset, greater involvement of the supraglottal structures than the epiglottis and lower risk of airway obstruction

DIFFERENTIAL DIAGONSIS Croup

Uvulitis

Bacterial tracheitis

Peritonsillar or retropharyngeal abscess

Foreign body in larynx or vallecular

Angioedema

Upper airway trauma or thermal injury

DIAGNOSIS ALOGRITHM

COMPLICATIONS Airway obstruction

Epiglotic abscess – May result from coaslescent epiglottic infection of secondary infection of epiglottic mucocele, occurs predominantly in adults and may complicate as many as 30% of cases

Secondary infection – pneumonia, cervical adenitis, cellulitis, septic arthritis, meningitis may result as a consequensce of bacteremia or direct extension

Necrotising epiglottitis – rare complication in immunocompromised patients

Death – mortality rate in children is <1% and in adults <3.3 percent, Death is almost always due to acute airway obstruction.

Most deaths occur en route to the hospital or soon thereafter

TREATMENT – GENERAL PRINCIPLES Maintainence of the airway

Administration of appropriate antimicrobial agents May be reasonable to withhold antibiotics in patients whose

epiglottitis is clearly known to be caused by inhalational, chemical or thermal injury

TREATMENT

Close monitoring

Humidified oxygen

The role of glucocorticoids in airway management of patients with epiglottitis is controversial

Management

Airway

In patients with moderate to severe respiratory distress, secure the airway in the operating room or similarly equipped setting (endotracheal tube or surgically if necessary) with an anesthesiologist and otolaryngologist present

If abrupt obstruction:

Attempt bag-valve mask ventilation first

During laryngoscopy, pressure on the chest by an assistant may produce bubbling and help indicate the location of the glottis

Perform needle cricothyrotomy or surgical cricothyrotomy if unable to ventilate or intubate*

Laboratory studies:

Epiglottal cultures after establishment of artificial airway

Blood cultures after the airway is secured

The role of glucocorticoids in airway management of patients with epiglottitis is controversial

ANTIMICROBIAL THERAPY Administer empiric antimicrobial therapy:

Cefotaxime OR ceftriaxone

PLUS

If community- or hospital-acquired Staphylococcus aureus is suspected, add clindamycin OR vancomycin based upon local antimicrobial susceptibility patterns

Monitor patient in the intensive care unit