EDITOR’S COMMENT

Remember: There is mandatory reporting to your local public health unit of some infectious diseases (see Table 47.2).

ANTIBIOTIC PRESCRIBING

A large volume of antibiotic prescriptions originate from the emergency department. To be responsible in your use of antibiotics, utilise up-to-date antibiotic guidelines and the infectious diseases and/or microbiology services in your hospital.

Antibiotic recommendations in this book are largely based on Therapeutic guidelines.¹

Don’t feel pressure to prescribe unnecessary antibiotics—most patients would prefer a thorough assessment and explanation of the medical condition, rather than an unnecessary antibiotic prescription.

Antibiotics are not harmless. They have side effects such as diarrhoea, allergic reactions and drug interactions, and they put pressure on antibiotic resistance in the community. We have already reached the era of untreatable multiresistant organisms and it is likely to get worse.

More often than not, there is sufficient time to discuss your antibiotic prescribing with a more senior emergency department clinician, the infectious diseases service or the hospital team that will be taking over care of your patient. Once an antibiotic is prescribed, it is rarely stopped, no matter how unnecessary it may be.

The antibiotic creed¹

M	Microbiology guides therapy wherever possible.
I	Indications should be evidence-based.
N	Narrowest spectrum required.
D	Dosage appropriate to the site and type of infection.
M	Minimise duration of therapy.
E	Ensure monotherapy in most situations.

Remember:

1. Patients on warfarin will need to have their international normalised ratio (INR) closely monitored.

2. Antibiotics can affect the absorption of the oral contraceptive pill (OCP). Recommend relevant patients use another form of contraception that month.

3. Patients are more likely to be adherent to the simplest antibiotic regimen (dosing regimen and pill count).

MULTI-RESISTANT STAPHYLOCOCCUS AUREUS (MRSA)

MRSA is resistant to beta-lactam and one or more other antibiotics. Initially it was only present in the healthcare setting, but now it has independently evolved in the community, hence the use of the term community-acquired MRSA (CA-MRSA) versus hospital-acquired MRSA (HA-MRSA).² It is all MRSA.

Some MRSA strains are sensitive to antibiotics such as clindamycin, doxycycline or trimethoprim + sulfamethoxazole and are therefore sometimes referred to as non-multi-resistant oxacillin-resistant Staphylococcus aureus (NORSA).² These strains manifest clinically as subcutaneous abscesses and necrotising pneumonia.

MRSA is now so prevalent in Australia that any staphylococcal infection needs to be thought of as potentially MRSA. Appropriate specimen collection is very important.

Management

Skin abscesses are managed by effective incision and drainage and rarely require antibiotics even when there is some surrounding erythema. If antibiotics are indicated, mild infection can be treated with a beta-lactam such as dicloxacillin while awaiting sensitivity results.¹

Severe infection, manifest as organ dysfunction, hypoperfusion or hypotension, needs treatment before sensitivities become available: vancomycin 1 g IV BD (adapted according to estimated glomerular filtration rate, eGFR).

SEPSIS

(See also ‘Septic shock’ in Chapter 11, ‘Shock’.)

• Sepsis is defined as infection with systemic inflammatory response.

• Severe sepsis is defined as sepsis with acute organ dysfunction.

• Septic shock (high mortality ~ 30%) is defined as:

• sepsis with hypotension refractory to initial fluid bolus

or

• evidence of tissue hypoperfusion (lactate > 4 mmol/L).

Early aggressive resuscitation in the emergency department has been shown to improve outcome.³

Management

1. Prompt fluid resuscitation—20–30 mL/kg fluid bolus on diagnosis.

2. Broad spectrum antibiotics within an hour after taking at least two sets of blood cultures simultaneously from different sites:⁴

• at least one set percutaneously

• at least one set from a vascular access device (if the device has been present > 48 hours)

• culture other sites as clinically indicated.

3. Insert central line and arterial line early.

Goals in the emergency department within 6 hours:⁴

1. Fluid resuscitation (crystalloid or colloid) to central venous pressure (CVP) 8–12 mmHg.

2. Mean arterial BP > 65 mmHg:

• vasopressor, e.g. noradrenaline, infusion once fluid resuscitated

• low-dose hydrocortisone for resistant hypotension.

3. Central venous oxygen saturation > 70% (sample from central venous catheter, CVC) or mixed venous sample > 65%:

• transfuse blood to haematocrit (HCT) ≥ 30% and/or

• dobutamine infusion (start at 2.5 μg/kg/min).

4. Take appropriate cultures and think about most likely source.

5. Treat the sepsis: broad spectrum antibiotics within an hour (ceftriaxone 2 g IV plus vancomycin 1 g IV if MRSA suspected).

6. Consult early with your infectious diseases service.

7. Source control of infection:

• drainage of abscess, debridement of tissue

• removal of foreign bodies, e.g. vascular access devices etc.

MENINGOCOCCAL INFECTION

Invasive meningococcal disease is life-threatening. The course can be fulminant with patients deteriorating within hours of onset of symptoms.

Neisseria meningitidis is a gram negative diplococcus with many serotypes. Serotypes B and C cause disease in Australia. Serotype C is now on the Australian childhood immunisation schedule. There is no vaccination available for serotype B.

Transmission is via asymptomatic nasal carriage (~ 10% population). Age groups 0–4 years and 15–25 years are most commonly affected by invasive disease with a seasonal peak in winter–spring.

Invasive infection can manifest as meningitis or more commonly as septicaemia (also referred to as meningococcaemia). Meningococcal meningitis has a high mortality rate of around 7%, but the mortality rate is even higher for meningococcal septicaemia at around 19%.

Management

Prehospital antibiotics in meningococcal sepsis can be life-saving^5,⁶—benzyl penicillin 30 mg/kg up to 1.2 g IM or IV or ceftriaxone 50 mg/kg up to 2 g IM or IV.

1. Ideally, draw blood cultures before giving antibiotics.

2. Antibiotics should be administered as soon as possible and within 30 minutes—ceftriaxone 2 g IV BD.⁵

3. If bacterial meningitis is suspected, dexamethasone 10 mg IV is recommended except in the patient with septic shock where high-dose steroids can be harmful. Low-dose hydrocortisone (50 mg IV qid) is an option in this situation.⁷

Investigations

• Send blood for meningococcal polymerase chain reaction (PCR) as well as culture.

• Send skin scrapings of purpuric lesions for gram stain and culture.

• Send cerebrospinal fluid (CSF) for culture and meningococcal PCR.

• Send blood for FBC, coagulation and biochemistry.

• Local public health unit needs to be notified ASAP (< 12 hours) for all cases where invasive meningococcal disease is being considered. Discuss with your infectious diseases service.

• Droplet transmission precautions should be instituted for 24 hours after commencement of antibiotics.

FEVER

Usually the cause of fever is apparent from other symptoms and signs, allowing focused investigation and management. First-line investigations such as urine culture, blood culture and chest X-ray may reveal an otherwise unapparent infective source.

When there is no apparent cause, a broad differential needs to be considered. Detailed and considered history taking, meticulous examination and tailored investigations are warranted.

Causes of fever can vary according to:

1. Age of patient:

• Elderly—

• Often do not mount much of a fever to a significant infection or may be hypothermic.

• Sepsis may manifest as confusion or decrease in function.

• Urosepsis and respiratory tract sepsis are common, but do not forget other potential sites.

• Paediatric (See Chapter 33, ‘Childhood emergencies’.)

2. Geography and travel history—see the section ‘Fever in the overseas traveller’ below.

Pyrexia of unknown origin (PUO)

Classic definition is fever > 38.3°C of unknown cause for 3 weeks despite initial medical consultation.

The decision needs to be made whether the patient requires inpatient or outpatient investigation and management.

Bacterial meningitis

In adults, 80% are Streptococcus pneumoniae or Neisseria meningitidis.

Clinical features

Of adult patients with bacterial meningitis, 95% present with two of the following:⁶

• fever

• headache

• neck stiffness

• change in mental status (Glasgow Coma Score (GCS) < 14).

Management

Early antibiotics improve outcome.⁷

1. Take blood cultures.

2. Ideally, perform lumbar puncture (LP) first also, but do not delay antibiotics. In patients where CT head is indicated prior to LP, administer dexamethasone and antibiotics prior to CT.

3. Antibiotics (ceftriaxone 2 g IV BD) should be administered within 30 minutes of clinical assessment.

4. Adjunctive dexamethasone therapy (10 mg IV prior/with antibiotics then q6h for 4 days) reduces mortality in bacterial meningitis, EXCEPT patients with concurrent septic shock where high dose steroids can be harmful. Low-dose hydrocortisone (50 mg qid) is an option.⁷

Streptococcus pneumoniae

Increasing penicillin/cephalosporin resistance depending on setting.

Management

• Consult microbiology service.

• If gram positive cocci on CSF gram stain, add vancomycin 500 mg IV q6h.

Herpes meningo-encephalitis

This is focal herpes simplex virus (HSV) infection of the cerebral cortex, especially the temporal lobe. Clinically, more neurological changes/seizures than bacterial meningitis.

Meningism is also present.

Request HSV PCR to be performed on CSF.

Treatment

Aciclovir 10 mg/kg IV q8h (adjusted for renal function).

Fever in the overseas traveller

Five important diagnoses to consider:

5. HIV (see Chapter 42, ‘The immunosuppressed patient’).

Viral hepatitis

Hepatitis A virus

• Acute self-limiting liver infection is transmitted by the faecal–oral route.

• Endemic in developing countries and immunisation is recommended for travellers.

• Incubation period of 2–7 weeks. Clinical features include flu-like symptoms, fever, fatigue, nausea then jaundice and dark urine. Clinically indistinguishable from other causes of acute hepatitis.

• Serological diagnosis.

• Management is supportive. Does not result in chronic hepatitis. Fulminant hepatitis is a rare complication. Immunoglobulin is used to control outbreaks in developed countries.

Hepatitis B virus (HBV)

This blood-borne virus is transmitted by parenteral or mucosal exposure to blood or bodily fluids.

Incubation period 1–4 months. Acute infection can be subclinical or non-specific hepatitis with flu-like symptoms, fatigue, nausea, right upper abdominal quadrant discomfort and jaundice. Liver transaminases can be elevated over 1000 IU/L. Markedly elevated prothrombin time can indicate development of fulminant liver failure.

HBV infection can be diagnosed by serology with the detection of hepatitis B surface antigen and IgM to core antigen. Hepatitis B DNA and hepatitis B e antigen are markers of viral replication. Hepatitis B DNA can be detected by PCR and can be used in fulminant hepatitis when hepatitis B surface antigen may still be undetectable.

Less than 1% will develop fulminant liver failure with acute hepatitis B infection. Antiviral therapy (lamivudine) is used by hepatologists to treat patients with severe or fulminant disease and an INR > 2. Transplant teams are also involved in these cases.

The presence of hepatitis B surface antigen beyond 6 months indicates persistent infection. Hepatitis B e antigen indicates viral replication. Viral load and response to therapy can be determined by quantitative hepatitis B DNA PCR. These patients can develop chronic hepatitis with the risk of progressing to cirrhosis and hepatocellular carcinoma.

Ninety-five percent of immunocompetent patients will clear the virus over 3–4 months, as indicated by normalisation of liver enzymes and loss of hepatitis B surface antigen which is replaced by hepatitis B surface antibodies. IgM core antibodies become IgG. Hepatitis B e antigen disappears and may be replaced by e antibody. Immunity as a result of past infection is indicated by these surface and core antibodies.

Immunisation results in development of surface antibody and has been part of the universal childhood vaccination program in Australia since 1996. Adults in high-risk groups, such as healthcare workers, are offered vaccination.

Hepatitis B immunoglobulin is also available and is used for passive immunity in non-immunised individuals following significant exposure to HBV-infected blood or bodily secretions. Vaccination is also commenced at this time. Be guided by your infectious diseases service, local postexposure prophylaxis guidelines and The Australian Immunisation Handbook (9^th edition, 2008).

Hepatitis C virus (HCV)

This blood-borne virus is transmitted predominantly by percutaneous exposure to infected blood. Prevalent in the injecting drug user population. Sexual contact and mother-to-infant transmission is much less common than with hepatitis B infection.

Acute infection is usually subclinical. Approximately 75% of those with acute HCV infection develop chronic hepatitis with the risk of cirrhosis and hepatocellular carcinoma. Treatment with interferon and ribavirin is successful in select patients. No vaccination is available.

Hepatitis D

This is found only in patients infected with hepatitis B. In developed countries, mostly found in injecting drug user population. Increases risk of fulminant hepatitis and sequelae of chronic hepatitis.

Hepatitis E

This is rare in developed countries. Enteric transmission. Usually causes self-limiting acute hepatitis, like hepatitis A, but fulminant disease is more common, particularly in pregnant women.

TRAVELlER’s DIARRHOEA

This is commonly caused by enterotoxigenic Escherichia coli.

Usually self-limiting illness and oral rehydration is sufficient management.

Antibiotics are associated with reduction of the duration and severity of the diarrhoea,⁹ and so can be used if the symptoms are not tolerable.

Management

1. Norfloxacin 800 mg PO single dose.¹⁰

2. If there is fever or blood in the diarrhoea, norfloxacin 400 mg PO bd for 3 days.¹⁰

3. Bloody diarrhoea needs to be referred to your gastroenterology service.

GASTROENTERITIS

• Typically, acute vomiting and non-bloody diarrhoea ± abdominal cramps.

• Most commonly a self-limiting viral or non-invasive bacterial infection.

• No role for stool culture in uncomplicated cases.

• No role for pathology testing in otherwise well adult with minimal dehydration.

Management

1. Hydration (oral or IV) is the cornerstone of management. Adults present to emergency department because they feel they are unable to tolerate liquid orally and feel significantly better after IV fluids ± an antiemetic ± antispasmodic.

2. Antidiarrhoeal agents can relieve stomach cramping and inconvenience. They should not be used in children, patients with inflammatory bowel disease or cases of invasive infection suggested by severe or bloody diarrhoea.

3. Loperamide 4 mg initially then 2 mg with each episode of diarrhoea up to 16 mg/day.

4. Patients with HIV infection require particular consideration (see Chapter 42, ‘The immunosuppressed patient’).

5. Bloody diarrhoea needs to be referred to your gastroenterology service.

Antibiotic-associated diarrhoea

Antibiotics often cause diarrhoea, particularly broad spectrum antibiotics such as amoxicillin + clavulanate. Consider Clostridium difficile infection and send stool for culture and C. difficile toxin detection.

Management

1. If C. difficile infection is proven or highly suspected, administer metronidazole 400 mg TDS for 7–10 days.

2. Infection control precautions will need to be initiated in the emergency department.

3. Relapse is common despite adherence to the regimen.

4. These patients should be referred to the gastroenterology or infectious diseases service.

TUBERCULOSIS (TB)

TB infects one-third of the world’s population and causes 2 million deaths a year. A resurgence of TB occurred with the onset of the HIV epidemic and continues. In 1993, WHO declared TB a global public health emergency.

In developed countries, TB is found in migrant populations from high prevalence countries and the itinerant population.

Prolonged exposure to infected respiratory droplets is usually required for transmission to occur, e.g. household contacts. Patients with acid fast bacilli seen on sputum smear are significantly more infectious than those without.

Cellular immunity develops 3–8 weeks following exposure, causing a positive tuberculin test, and immune response causes limitation of further infection. TB can remain dormant for many years, ‘latent TB infection’ (LTBI), and may reactivate with immunodeficiency, immunosuppression and immunocompromise (including senescence of old age). In general, after exposure to TB infection, there is considered to be about a 5% lifetime risk of developing disease. The first half of this risk (2.5%) is for progression to TB disease within 2 years of exposure. The other 2.5% risk is conferred lifelong, with an increasing risk in old age.

Progressive primary infection can occur in the very young and immunocompromised/deficient/suppressed. Uncontrolled haematogenous spread causes disseminated disease with widespread lung involvement (miliary TB).

Clinical features

• Anorexia, weight loss, fatigue

• Fever, night sweats

• Cough with purulent sputum ± haemoptysis

• Pleural effusion/consolidation

• Normochromic, normocytic anaemia

• Raised inflammatory markers

Note: Migration from a high-prevalence country and symptoms of cough > 3 weeks with systemic features is highly suggestive of TB infection. Extrapulmonary TB may also occur, and should be carefully considered in patients with a chronic illness from a high TB prevalence country.

Management

TB is a notifiable disease that needs specialist management. Concurrent HIV infection needs to be considered. Contact tracing and prophylactic treatment of household contacts is performed by public health staff. Respiratory isolation/infection control should be initiated if TB is in the differential diagnosis to simplify public health measures once the diagnosis is confirmed.

TETANUS

Clostridium tetani is an anaerobic gram negative rod found in soil that produces tetanospasmin toxin (tetanus toxin). Tetanus toxin binds cells in the nervous system, blocking inhibition of motor neurons and sympathetic fibres, causing the clinical manifestations of the disease.

Route of infection is commonly via contaminated puncture or laceration wounds that contain an anaerobic environment as a result of devitalised tissue. Tetanus is a preventable disease through immunisation and wound care.

Tetanus does occur in developed countries, although rarely. There has been increased incidence in patients over 60 years of age, which is thought to be related to waning immunity. Occurs in developing countries particularly in neonates, due to septic birth practices and lack of immunisation.

Generalised tetanus:

• Initial symptoms are masseter muscle spasm ‘lockjaw’ and obicularis oris hypertonia ‘risus sardonicus’.

• Progresses to opisthotonic decorticate posturing.

• Patient is fully conscious and it is severely painful.

• Spasms are triggered by sensory stimuli.

• Spasm can stop respiration and obstruct the airway.

• Autonomic dysfunction.

Localised tetanus:

• Muscle spasms at site of inoculation reflect partial immunity or prodrome to generalised tetanus.

Diagnosis

• Tetanus is a clinical diagnosis.

• Difficult to culture and antibody levels not diagnostic.

• Differential includes:

• strychnine poisoning—mimics it clearly, also occurs in injecting drug users, initial supportive management is the same

• dystonic reactions

• dental infections.

SKIN SEPSIS

(Also see Chapter 40, ‘Dermatological presentations to emergency’.)

Infectious cellulitis

Commonly seen in the leg in adults. Bilateral cellulitis is rare.

Wound-associated cellulitis is usually due to S. aureus whereas ‘spontaneous’ cellulitis is usually group A streptococcal infection. Tinea pedis between toes is a common entry site.

Examination reveals erythema with or without lymphangitis. There may be enlarged and tender draining lymph nodes.

Rapidly progressing infections (gangrenous cellulitis)

Necrosis of the soft tissues can spread rapidly and be limb- and life-threatening.

• Can be polymicrobial e.g.: Fournier’s gangrene, necrotising fasciitis of scrotum that can progress to perineum, penis and abdominal wall.

• Can be a single microbe e.g.:

• Clostridium myonecrosis (gas gangrene),

• Streptococcus pyogenes, Staphylococcus aureus

• water-related infections.

Clinical features

• Marked systemic toxicity out of proportion to local findings

• Erythema, swelling, indiscrete margins

• Very tender initially

• Crepitus cellulitis

• Anaesthesia of overlying skin

• Rapid spread (can spread widely in deep fascial planes with relative sparing of overlying skin)

• Systemic toxicity ± septic shock

Management

1. Needs urgent debridement of necrotic tissue and early antibiotics.

2. Consult surgeons and infectious diseases services early in your management.

3. Meropenem 1 g IV q8h plus clindamycin 600 mg IV q8h.

WOUND INFECTIONS

(Also see Chapter 40, ‘Dermatological presentations to emergency’.)

These are usually related to skin organisms and can be managed as for cellulitis.

Remove any foreign material such as sutures and clean/debride as appropriate.

Some special circumstances are included under the following sections.

Penetrating wounds through footwear

Pseudomonas infection is common.

Treatment

Ciprofloxacin 500 mg PO BD for 5 days

WATER-RELATED INFECTIONS

These are complicated infections and advice should be sought from your infectious diseases service.

Management

1. Salt water exposure with cellulitis/bullous lesions or necrotic ulcers—consider Vibrio species infection. Administer doxycycline 200 mg stat, then 100 mg BD for 5 days.

2. Fresh water infection can be Aeromonas infection. Administer ciprofloxacin 500 mg PO BD for 5 days.

3. Coral cut infections are often caused by Streptococcus pyogenes which is sensitive to penicillin and so can be managed as for uncomplicated cellulitis.

4. Fish tank water:

• Mycobacterium marinum can cause papular lesions.

• Requires referral for biopsy and infectious diseases expertise.

HERPES ZOSTER (SHINGLES)

Reactivation of varicella (chickenpox) manifesting as a vesicular rash in a dermatomal distribution. A prodrome may precede the appearance of vesicles, e.g. pain, an ‘itchy’ or other abnormal sensation at the site.

If more than one dermatome is involved or disease is disseminated, consider underlying immunosuppression/compromise/deficiency.

Management

Antiviral therapy can reduce symptoms if commenced within 72 hours of rash onset:

• famciclovir 250 mg TDS for 7 days

or

• valaciclovir 1 g TDS for 7 days

or

• aciclovir 800 mg 5 times a day for 7 days.

First division of trigeminal nerve requires special consideration as the cornea can be involved—consult ophthalmologist.

SEXUALLY TRANSMITTED INFECTION (STI)

Presence of one STI implies potential exposure to every other STI and pregnancy. All patients need referral to a sexual health clinic where follow-up, contact tracing, counselling and education can occur.

Commencing treatment in emergency department may have important public health benefits.

Presenting complaints include:

• genital lesions

• vaginitis/vaginal/urethral discharge or dysuria

• pelvic pain in women.

Genital lesions

Wart-like lesions

• Human papilloma virus.

• Clinical diagnosis.

• Refer to sexual health clinic, gynaecologist or urologist for management.

Itchy lesions

Don’t forget scabies and lice!

Management

Topical treatments available over-the-counter are usually sufficient. Patient’s clothing and bedding should be laundered.

Transmission generally requires prolonged skin-to-skin contact.

Vulvovaginitis

Inflamed, irritated vagina/labia with discharge.

Management

1. If discharge is from cervix, manage as for cervicitis.

2. If there is pelvic tenderness, manage as for PID.

3. Send swab for culture.

Trichomonas

• Not normal flora—sexually transmitted

• Purulent malodorous discharge

• Linked with pregnancy complications

Treatment

Metronidazole 2 g PO single dose

Bacterial vaginosis

• Polymicrobial overgrowth with anaerobes

• Generally not sexually transmitted

• Treat if symptomatic

Treatment

Metronidazole 400 mg BD for 7 days

Epididymo-orchitis

Secondary to urinary tract infection or sexually transmitted disease.

Management

• If sexually transmitted, manage as for urethritis and refer to sexual health service.

• Otherwise manage as per urinary tract infection in men.

Balanitis

• In uncircumcised males.

• In adult males it is usually candida.

Management

• Swab and treat with combined anticandidal and steroid cream.

• Continue treatment for 2 weeks after symptoms resolve.

Pelvic pain in women

Always exclude pregnancy by testing urine or blood regardless of the history given.

Pelvic inflammatory disease (PID)

• 13% of women are infertile after a single episode.

• Risk of ectopic pregnancy increases 7-fold after one episode.

• Can also lead to pelvic adhesions and chronic pelvic pain.

Treatment

1. Azithromycin 1 g PO on day 1 and day 8 + ceftriaxone 250 mg IM or IV stat + metronidazole 400 mg BD for 14 days.

2. Severe infection: azithromycin 1 g PO or IV on day 1 and day 8 + ceftriaxone 1 g IV daily + metronidazole 500 mg IV BD.

3. All women with PID should be referred to a gynaecologist.

Note: Ensure women realise that a speculum examination in this setting does not include a Pap smear. This will need to be done by their GP once any infection has subsided.

URINARY TRACT INFECTION

Asymptomatic bacteriuria need not be treated except in pregnant women.

Asymptomatic bacteriuria is quite common in elderly patients, but be aware that symptoms can be non-specific such as confusion or a decrease in general function.

Uncomplicated lower urinary tract infection (UTI)

Acute pyelonephritis

• Symptoms of upper urinary tract infection include:

• fever often with rigors/chills

• flank pain—bilateral or unilateral

• dysuria

• Pregnant women can develop severe infection:

• ureters physiologically dilated in pregnancy

• associated with adverse pregnancy outcomes.

• Pyelonephritis is more common in patients with diabetes.

• Can develop emphysematous pyelonephritis:

• high mortality ~70% and is a medical emergency

• requires urgent nephrectomy.

Investigations

• Send urine and blood for culture.

• Imaging:

• Routine imaging is NOT necessary in uncomplicated pyelonephritis.

• Renal ultrasound should be performed in pregnant women, diabetics, men.

• Renal ultrasound should be performed if flank pain is severe, unresponsive to therapy, impaired renal function.

Catheters

• Asymptomatic bacteriuria and pyuria is common with long-term catheterisation.

• Should only be treated if symptomatic.

• Catheter change or removal is essential if treatment for a catheter-associated UTI is considered necessary.

BODY FLUIDS EXPOSURE AND NEEDLE STICK INJURIES

Follow protocols within your health care facility.

(See also ‘Post-exposure prophylaxis’ in Chapter 42, ‘The immunosuppressed patient’.)

Community needle stick injuries:

• Risk of HIV transmission is so low that it is not measurable.

• Tetanus prophylaxis is indicated.

Principles

1. Immediate treatment:

a. Wash skin and wounds with water or saline.

b. Irrigate mucous membranes/eyes (remove contacts) with water or saline.

c. Spit out blood/bodily fluids and rinse mouth with water.

d. Do not douche the vagina or rectum.

3. Baseline testing of recipient:

a. Depending on risk assessment and method of exposure—

• may include HIV antibody test, HBV and HCV serology, STI screen, pregnancy test

• FBC, LFT, electrolytes for patients commencing PEP

b. Testing always requires appropriate counselling and follow up

4. Prescription of prophylactic medication and immunisations:¹¹

a. Consider—

• HIV, HBV, HCV (see below)

• tetanus immunisation

• prophylactic STI treatments if there is known or high risk of STI, or suspected non-compliance with follow-up

• pregnancy in unprotected sexual exposure in women

5. Counselling and follow–up:

a. e.g., referral to occupational health service

b. sexual health service

Hepatitis B

• Commence vaccination schedule in the non-immunised.¹² Where vaccination has occurred but immune response is unknown, test for hepatitis B surface antibody level.

• Consider giving HBV immunoglobulin to non-immune individual within 72 hours if the source is, or strongly suspected to be, infected with hepatitis B.

• Discuss with your infectious diseases service.