Swine Flu - Clinical Management National Guidelines INDIA

Swine Flu

Clinical management Protocol

and

Infection Control Guidelines

Directorate General of Health Services

Ministry of Health and Family Welfare

Government of India

Swine Influenza

Clinical Management Protocol



1. Introduction
As on 30.04.09, 148 laboratory confirmed human cases of Swine influenza A (H1N1) has been reported from nine countries with 8 deaths. ( Mexico [26 cases, 7 deaths], USA [91 cases, one death], Canada (13), Austria(1), Germany (3), Israel(2), New Zealand (3), Spain(4), and United Kingdom (5). Over 1300 suspected cases have been reported with about 100 deaths. The outbreak started in Mexico on 18th March, 2009 and spread to USA and Canada and then to other countries.

WHO has heightened the pandemic level to Phase 5 implying widespread human infection.





2. Epidemiology



2.1 The agent



Genetic sequencing shows a new sub type of influenza A (H1N1) virus with segments from four influenza viruses: North American Swine, North American Avian, Human Influenza and Eurasian Swine.



2.2Host factors



The majority of these cases have occurred in otherwise healthy young adults.



2.3Transmission



The transmission is by droplet infection and fomites.



2.4 Incubation period



1-7 days.



2.5 Communicability



From 1 day before to 7 days after the onset of symptoms. If illness persist for more than 7 days, chances of communicability may persist till resolution of illness. Children may spread the virus for a longer period.



There is substantial gap in the epidemiology of the novel virus which got re-assorted from swine influenza.



3. Clinical features



Important clinical features of swine influenza include fever, and upper respiratory symptoms such as cough and sore throat. Head ache, body ache, fatigue diarrhea and vomiting have also been observed.



There is insufficient information to date about clinical complications of this variant of swine origin influenza A (H1N1) virus infection. Clinicians should expect complications to be similar to seasonal influenza: sinusitis, otitis media, croup, pneumonia, bronchiolitis, status asthamaticus, myocarditis, pericarditis, myositis, rhabdomyolysis, encephalitis, seizures, toxic shock syndrome and secondary bacterial pneumonia with or without sepsis. Individuals at extremes of age and with preexisting medical conditions are at higher risk of complications and exacerbation of the underlying conditions.



The reporting of cases is to be based on the case definition provided (Annexure-I).





4. Investigations



Routine investigations required for evaluation and management of a patient with symptoms as described above will be required. These may include haematological, biochemical, radiological and microbiological tests as necessary.

Confirmation of influenza A(H1N1) swine origin infection is through:

Real time RT PCR or

Isolation of the virus in culture or

Four-fold rise in virus specific neutralizing antibodies.

For confirmation of diagnosis, clinical specimens such as nasopharyngeal swab, throat swab, nasal swab, wash or aspirate, and tracheal aspirate (for intubated patients) are to be obtained. The sample should be collected by a trained physician / microbiologist preferably before administration of the anti-viral drug. Keep specimens at 4°C in viral transport media until transported for testing. The samples should be transported to designated laboratories with in 24 hours. If they cannot be transported then it needs to b stored at -70°C. Paired blood samples at an interval of 14 days for serological testing should also be collected.

5. Treatment



The guiding principles are:



Early implementation of infection control precautions to minimize nosocomical / household spread of disease

Prompt treatment to prevent severe illness & death.

Early identification and follow up of persons at risk.



5.1 Infrastructure / manpower / material support



Isolation facilities: if dedicated isolation room is not available then patients can be cohorted in a well ventilated isolation ward with beds kept one metre apart.

Manpower: Dedicated doctors, nurses and paramedical workers.

Equipment: Portable X Ray machine, ventilators, large oxygen cylinders, pulse oxymeter

Supplies: Adequate quantities of PPE, disinfectants and medications (Oseltamivir, antibiotics and other medicines)



5.2Standard Operating Procedures



Reinforce standard infection control precautions i.e. all those entering the room must use high efficiency masks, gowns, goggles, gloves, cap and shoe cover.

Restrict number of visitors and provide them with PPE.

Provide antiviral prophylaxis to health care personnel managing the case and ask them to monitor their own health twice a day.

Dispose waste properly by placing it in sealed impermeable bags labeled as Bio- Hazard.



5.3Oseltamivir Medication



Oseltamivir is the recommended drug both for prophylaxis and treatment.



Dose for treatment is as follows:

By Weight:

For weight <15kg 30 mg BD for 5 days

15-23kg 45 mg BD for 5 days

24-<40kg 60 mg BD for 5 days

>40kg 75 mg BD for 5 days

For infants:

< 3 months 12 mg BD for 5 days

3-5 months 20 mg BD for 5 days

6-11 months 25 mg BD for 5 days

It is also available as syrup (12mg per ml )

If needed dose & duration can be modified as per clinical condition.

Adverse reactions:

Oseltamivir is generally well tolerated, gastrointestinal side effects (transient nausea, vomiting) may increase with increasing doses, particularly above 300 mg/day. Occasionally it may cause bronchitis, insomnia and vertigo. Less commonly angina, pseudo membranous colitis and peritonsillar abscess have also been reported. There have been rare reports of anaphylaxis and skin rashes. In children, most frequently reported side effect is vomiting. Infrequently, abdominal pain, epistaxis, bronchitis, otitis media, dermatitis and conjunctivitis have also been observed. There is no recommendation for dose reduction in patients with hepatic disease. Though rare reporting of fatal neuro-psychiatiric illness in children and adolescents have been linked to oseltamivir, there is no scientific evidence for a causal relationship.



5.4Supportive therapy



IV Fluids.

Parentral nutrition.

Oxygen therapy/ ventilatory support.

Antibiotics for secondary infection.

Vasopressors for shock.

Paracetamol or ibuprofen is prescribed for fever, myalgia and headache. Patient is advised to drink plenty of fluids. Smokers should avoid smoking. For sore throat, short course of topical decongestants, saline nasal drops, throat lozenges and steam inhalation may be beneficial.

Salicylate / aspirin is strictly contra-indicated in any influenza patient due to its potential to cause Reye’s syndrome.

The suspected cases would be constantly monitored for clinical / radiological evidence of lower respiratory tract infection and for hypoxia (respiratory rate, oxygen saturation, level of consciousness).

Patients with signs of tachypnea, dyspnea, respiratory distress and oxygen saturation less than 90 per cent should be supplemented with oxygen therapy. Types of oxygen devices depend on the severity of hypoxic conditions which can be started from oxygen cannula, simple mask, partial re-breathing mask (mask with reservoir bag) and non re-breathing mask. In children, oxygen hood or head boxes can be used.

Patients with severe pneumonia and acute respiratory failure (SpO2 < 90% and PaO2 <60 mmHg with oxygen therapy) must be supported with mechanical ventilation. Invasive mechanical ventilation is preferred choice. Non invasive ventilation is an option when mechanical ventilation is not available. To reduce spread of infectious aerosols, use of HEPA filters on expiratory ports of the ventilator circuit / high flow oxygen masks is recommended.

Maintain airway, breathing and circulation (ABC);

Maintain hydration, electrolyte balance and nutrition.

If the laboratory reports are negative, the patient would be discharged after giving full course of oseltamivir. Even if the test results are negative, all cases with strong epidemiological criteria need to be followed up.

Immunomodulating drugs has not been found to be beneficial in treatment of ARDS or sepsis associated multi organ failure. High dose corticosteroids in particular have no evidence of benefit and there is potential for harm. Low dose corticosteroids (Hydrocortisone 200-400 mg/ day) may be useful in persisting septic shock (SBP < 90).

Suspected case not having pneumonia do not require antibiotic therapy. Antibacterial agents should be administered, if required, as per locally accepted clinical practice guidelines. Patient on mechanical ventilation should be administered antibiotics prophylactically to prevent hospital associated infections.



5.5 Discharge Policy



Adult patients should be discharged 7 days after symptoms have subsided.

Children should be discharged 14 days after symptoms have subsided.

The family of patients discharged earlier should be educated on personal hygiene and infection control measures at home; children should not attend school during this period.



5.6 Chemo Prophylaxis



All close contacts of suspected, probable and confirmed cases. Close contacts include household /social contacts, family members, workplace or school contacts, fellow travelers etc.

All health care personnel coming in contact with suspected, probable or confirmed cases

Oseltamivir is the drug of choice.

Prophylaxis should be provided till 10 days after last exposure (maximum period of 6 weeks)

By Weight:

For weight <15kg 30 mg OD

15-23kg 45 mg OD

24-<40kg 60 mg OD

>40kg 75 mg OD

For infants:

< 3 months not recommended unless situation judged critical due to limited data on use in this age group

3-5 months 20 mg OD

6-11 months 25 mg OD











5.7 Non-Pharmaceutical Interventions



Close Contacts of suspected, probable and confirmed cases should be advised to remain at home (voluntary home quarantine) for at least 7 days after the last contact with the case. Monitoring of fever should be done for at least 7 days. Prompt testing and hospitalization must be done when symptoms are reported.

All suspected cases, clusters of ILI/SARI cases need to be notified to the State Health Authorities and the Ministry of Health & Family Welfare, Govt. of India (Director, EMR and NICD)



6. Laboratory Tests

The samples are to be tested in BSL-3 laboratory. At present the following laboratories are the identified laboratories for this purpose:

(i)National Institute of Communicable Diseases, 22, Sham Nath Marg, Delhi [Tel. Nos. Influenza Monitoring Cell: 011-23921401; Director: 011-23913148]

(ii)National Institute of Virology, 20-A, Dr. Ambedkar Road, Pune-411001 [Tel.No. 020-26124386]



Guidelines on Infection control Measures



Infection control measures would be targeted according to the risk profile as follows:



1. Health facility managing the human cases of avian influenza



1.1During Pre Hospital Care



Standard precautions are to be followed while transporting patient to a health-care facility. The patient should also wear a three layer surgical mask.

Aerosol generating procedures should be avoided during transportation as far as possible.

The personnel in the patient’s cabin of the ambulance should wear full complement of PPE including N95 masks, the driver should wear three layered surgical mask.

Once the patient is admitted to the hospital, the interior and exterior of the ambulance and reusable patient care equipment needs to be sanitized using sodium hypochlorite / quaternary ammonium compounds.

Recommended procedures for disposal of waste (including PPE used by personnel) generated in the ambulance while transporting the patient should be followed.





1.2 During Hospital Care



The patient should be admitted directly to the isolation facility and continue to wear a three layer surgical mask.

The identified medical, nursing and paramedical personnel attending the suspect/ probable / confirmed case should wear full complement of PPE (including N95 mask). If splashing with blood or other body fluids is anticipated, a water proof apron should be worn over the PPE.

Aerosol-generating procedures such as endotracheal intubation, nebulized medication administration, induction and aspiration of sputum or other respiratory secretions, airway suction, chest physiotherapy and positive pressure ventilation should be performed by the treating physician/ nurse wearing full complement of PPE with N95 respirator on.

Sample collection and packing should be done under full cover of PPE.

Perform hand hygiene before and after patient contact and following contact with contaminated items, whether or not gloves are worn.

Until further evidence is available, infection control precautions should continue in an adult patient for 7 days after resolution of symptoms and 14 days after resolution of symptoms for children younger than 12 years because of longer period of viral shedding expected in children. If the patient insists on returning home, after resolution of fever, it may be considered, provided the patient and household members follow recommended infection control measures and the cases could be monitored by the health workers in the community.

The virus can survive in the environment for variable periods of time (hours to days). Cleaning followed by disinfection should be done for contaminated surfaces and equipments.

The virus is inactivated by a number of disinfectants such as 70% ethanol, 5% benzalkonium chloride (Lysol) and 10% sodium hypochlorite. Patient rooms/areas should be cleaned at least daily and finally after discharge of patient. In addition to daily cleaning of floors and other horizontal surfaces, special attention should be given to cleaning and disinfecting frequently touched surfaces. To avoid possible aerosolization of the virus, damp sweeping should be performed. Horizontal surfaces should be dusted by moistening a cloth with a small amount of disinfectant.

Clean heavily soiled equipment and then apply a disinfectant effective against influenza virus (mentioned above) before removing it from the isolation room/area. If possible, place contaminated patient-care equipment in suitable bags before removing it from the isolation room/area.

When transporting contaminated patient-care equipment outside the isolation room/area, use gloves followed by hand hygiene. Use standard precautions and follow current recommendations for cleaning and disinfection or sterilization of reusable patient-care equipment.

All waste generated from influenza patients in isolation room/area should be considered as clinical infectious waste and should be treated and disposed in accordance with national regulations pertaining to such waste. When transporting waste outside the isolation room/area, gloves should be used followed by hand hygiene.



Annexure I





Case Definition





A suspected case of swine influenza A (H1N1) virus infection is defined as a person

with acute febrile respiratory illness (fever ≥ 38 0 C) with onset.:

within 7 days of close contact with a person who is a confirmed case of swine influenza A (H1N1) virus infection, or

 within 7 days of travel to community where there are one or more confirmed swine influenza A(H1N1) cases, or

resides in a community where there are one or more confirmed swine influenza cases.

A probable case of swine influenza A (H1N1) virus infection is defined as a person with an acute febrile respiratory illness who:

is positive for influenza A, but unsubtypable for H1 and H3 by influenza RT-PCR or reagents used to detect seasonal influenza virus infection, or

is positive for influenza A by an influenza rapid test or an influenza immunofluorescence assay (IFA) plus meets criteria for a suspected case

individual with a clinically compatible illness who died of an unexplained acute respiratory –illness who is considered to be epidemiologically linked to a probable or confirmed case.

A confirmed case of swine influenza A (H1N1) virus infection is defined as a person with an acute febrile respiratory illness with laboratory confirmed swine influenza A (H1N1) virus infection at WHO approved laboratories by one or more of the following tests:



Real Time PCR

viral culture

Four-fold rise in swine influenza A (H1N1) virus specific neutralizing antibodies.





Annexure II







Standard Operating Procedures on Use of PPE





Personal Protection Equipments



PPE reduces the risk of infection if used correctly. It includes:

• Gloves (nonsterile),

• Mask (high-efficiency mask) / Three layered surgical mask,

• Long-sleeved cuffed gown,

• Protective eyewear (goggles/visors/face shields),

• Cap (may be used in high risk situations where there may be increased

aerosols),

• Plastic apron if splashing of blood, body fluids, excretions and secretions is

anticipated.





Goggles N-95 Mask

OR





Gown(must for lab work) Triple layer Mask



Gloves Shoe covers



The PPE should be used in situations were regular work practice requires unavoidable, relatively closed contact with the suspected human case / poultry.



Correct procedure for applying PPE in the following order:



1.Follow thorough hand wash

2.Wear the coverall.

3.Wear the goggles/ shoe cover/and head cover in that order.

4.Wear face mask

5.Wear gloves



The masks should be changed after every six to eight hours.



Remove PPE in the following order:



• Remove gown (place in rubbish bin).

• Remove gloves (peel from hand and discard into rubbish bin).

• Use alcohol-based hand-rub or wash hands with soap and water.

• Remove cap and face shield (place cap in bin and if reusable place face shield in container for decontamination).

• Remove mask - by grasping elastic behind ears – do not touch front of mask

• Use alcohol-based hand-rub or wash hands with soap and water.

• Leave the room.

• Once outside room use alcohol hand-rub again or wash hands with soap and water.













Annexure III



Guidelines/ operating procedures for infection control practices



1. Infection control measures at Individual level

1.1 Hand Hygiene



Hand hygiene is the single most important measure to reduce the risk of transmitting infectious organism from one person to other.



Hands should be washed frequently with soap and water / alcohol based hand rubs/ antiseptic hand wash and thoroughly dried preferably using disposable tissue/ paper/ towel.



After contact with respiratory secretions or such contaminated surfaces.

Any activity that involves hand to face contact such as eating/ normal grooming / smoking etc.





Steps of hand washing







Step 1. Step 2.

Wash palms and fingers. Wash back of hands.











Step 3. Step 4.

Wash fingers and knuckles. Wash thumbs.















Step 5. Step 6.

Wash fingertips. Wash wrists.





1.2 Respiratory Hygiene/Cough Etiquette



The following measures to contain respiratory secretions are recommended for all individuals with signs and symptoms of a respiratory infection.



Cover the nose/mouth with a handkerchief/ tissue paper when coughing or sneezing;

Use tissues to contain respiratory secretions and dispose of them in the nearest waste receptacle after use;

Perform hand hygiene (e.g., hand washing with non-antimicrobial soap and water, alcohol-based hand rub, or antiseptic hand wash) after having contact with respiratory secretions and contaminated objects/materials





1.3Staying away



Stay away from poultry. Keep them secure in cages. Keep children out of reach.

Wash hands if in contact with poultry or poultry products.

Stay at least one metre away from a person having cough or sneeze.



1.4 Use of mask



As there is no efficient human to human transmission in phase III, masks are not recommended for individuals or community. As a matter of abundant precaution, PUI/ suspected cases managed at home and there family contacts are trained on using three layered surgical masks.

2. Infection control measures at health facility

2.1 Droplet Precautions:



Advise healthcare personnel to observe Droplet Precautions (i.e., wearing a surgical or procedure masks for close contact), in addition to Standard Precautions, when examining a patient with symptoms of a respiratory infection, particularly if fever is present. These precautions should be maintained until it is determined that the cause of symptoms is not an infectious agent that requires Droplet Precautions.



2.2 Visual Alerts



Post visual alerts (in appropriate languages) at the entrance to outpatient facilities (e.g., emergency departments, physician offices, outpatient, clinics) instructing patients and persons who accompany them (e.g., family, friends) to inform healthcare personnel of symptoms of a respiratory infection when they first register or care and to practice Respiratory Hygiene/Cough Etiquette.



2.3 Use of PPE





The medical, nurses and paramedics attending the suspect/ probable / confirmed case should wear full complement of PPE (Annexure-IX).

Use N-95 masks during aerosol-generating procedures.

Perform hand hygiene before and after patient contact and following contact with contaminated items, whether or not gloves are worn.

Sample collection and packing should be done under full cover of PPE.



2.4 Decontaminating contaminated surfaces, fomites and equipments



Cleaning followed by disinfection should be done for contaminated surfaces and equipments.

use phenolic disinfectants, quaternary ammonia compounds , alcohol or sodium hypochlorite. Patient rooms/areas should be cleaned at least daily and terminally after discharge. In addition to daily cleaning of floors and other horizontal surfaces, special attention should be given to cleaning and disinfecting frequently touched surfaces.

To avoid possible aerosolization of AI virus, damp sweeping should be performed.

Clean heavily soiled equipment and then apply a disinfectant effective against influenza virus before removing it from the isolation room/area.

When transporting contaminated patient-care equipment outside the isolation room/area, use gloves followed by hand hygiene. Use standard precautions and follow current recommendations for cleaning and disinfection or sterilization of reusable patient-care equipment.



2.5 Guidelines for waste disposal



All the waste has to be treated as infectious waste and decontaminated as per standard procedures

Articles like swabs/gauges etc are to be discarded in the Yellow coloured autoclavable biosafety bags after use, the bags are to be autoclaved followed by incineration of the contents of the bag.

Waste like used gloves, face masks and disposable syringes etc are to be discarded in Blue/White autoclavable biosafety bags which should be autocalaved/microwaved before disposal

All hospitals and laboratory personnel should follow the standard guidelines (Biomedical waste management and handling rules, 1998) for waste management.

Swine Flu - Guidelines for testing.

Revised Guidelines for testing of persons with flu like symptoms reporting at hospitals notified for influenza H1N1




So far, the present guidelines stipulate that a person suspected of influenza A H1N1 need to be referred to an identified govt. health facility. He/she needs to be kept in an isolation facility in that hospital and if found positive, is treated accordingly.

In order to make the testing facility for H1N1 more accessible at large and due to the onset of the Influenza season in the country, it has been decided to revise the existing guidelines.

Under the new guidelines, any person with flu like symptoms such as fever, cough, sore throat, cold, running nose etc. should go to a designated Government facility for giving his/her sample for testing for the H1N1 virus. After clinical assessment, the designated medical officer would decide on the need for testing. Except for cases that are severe, the patient would be allowed to go home (This was not allowed under the existing guidelines).

The sample of the suspect case would be collected and sent to the notified laboratory for testing. If tested as positive for H1N1 and in case the symptoms are mild, the patient would be informed and given the option of admission into the hospital or isolation and treatment at his own home.

In case the patient opts for home isolation and treatment, he/she would be provided with detailed guidelines / safety measures to be strictly adhered to by the entire household of the patient. He/ she would have to provide full contact details of his entire household. The house hold and social contacts would be provided with the preventive treatment.

Notwithstanding the above guidelines, the decision of the doctor of the notified hospital about admitting the patient would be final.



In case the test is negative, the patient will accordingly be informed.

These guidelines have been issued by the Government in public interest and shall be reviewed from time to time depending on the spread of the pandemic and its severity in the country. These guidelines would however not apply to passengers who are identified through screening at the points of entry. The existing policy of isolating passengers with flu like symptoms would continue.

Drowning and Near Drowning: Submersion Injuries

Drowning and Near Drowning: Submersion Injuries






Submersion injuries are the second leading cause of accidental death in children. A drowning event is a fatal submersion injury; a near-drowning event is one in which the victim survives, albeit possibly with important disabilities. In the US, submersion events account for approximately 1000 deaths and more than 3000 emergency department visits annually for children <19 years of age (1,35). Despite advances in medical care and efforts to prevent such events, outcomes from all but brief submersion events remain, in many cases, quite poor.



Epidemiology

Most submersions occur in fresh water, with a large proportion of these occurring in natural bodies of water—rivers, creeks, lakes, and ponds. Submersions also occur frequently in domestic sites—home pools, spas, or bathtubs—and recreational community pools, water parks, schools, etc. (19). An investigation of specific drowning sites in the US demonstrated that, for the country as a whole, as few as 4% of events occur in salt water, although this incidence is higher in coastal communities (8).



Three groups of children are at particular risk for submersion injuries: the very young, adolescent males, and nonwhites. Submersion events that involve infants and toddlers commonly occur in sources of water in the home (8). Infants who are 6–11 months of age largely drown in bathtubs, and the use of infant bathtub seats does not prevent such events (9). Older infants and toddlers may drown as the result of a fall into a shallow body of water such as a wading pool, spa, or bathtub (3,8,38). Moreover, infants and toddlers are the group least likely to have a witnessed drowning event (38), a condition associated with longer submersion time and poorer outcomes. In this age group, males and females drown with equal frequency; in all other age groups, submersion event rates are higher in males than in females (8,38).



Boys who are 15–19 years of age have the second highest drowning rate. Events in this age group are generally related to recreational water activities. This population has the highest rate of drowning while swimming, boating, or driving a car, even when compared with adults who, over a lifetime, engage in such activities to a greater extent (38). African American boys have a higher drowning incidence with such events usually recreation related. A fourfold increased incidence in 5–9-year-old and a >10-fold increased incidence in 15–19-year-old African American males have been demonstrated, as compared with their Caucasian counterparts (8). Moreover, fatal submersion injuries are higher in African Americans and Hispanics in than the general pediatric population (25).

Certain medical conditions may predispose children to submersion (Table 28.1). Drowning risk is elevated in children with epilepsy, with the highest number of events occurring in bathtubs and pools (15). Epilepsy, excluding other neurologic disabilities, results in a 10-fold increased risk of submersion events (15). In one report, 7% of pediatric drowning victims had a prior history of seizure (38). Hyperventilation with swimming exertion may even predispose a child with epilepsy to have a seizure, thus precipitating the drowning event.



Patients with long QT syndrome (LQTS) or other cardiac “channelopathies” are at increased risk for drowning events (2,7,11). Ventricular tachyarrhythmias in such patients may be exacerbated by swimming. In one report, 91% of patients who presented for evaluation of possible LQTS and had personal or family history of swimming-related syncope had mutations in the LQTS1 gene (11). Swimming is an arrhythmogenic trigger because the action activates the “diving reflex,” which alters autonomic stability. This diving reflex is elicited in mammals by contact of the face with cold water and consists of breath-holding, bradycardia, and intense peripheral vasoconstriction. Swimming also involves physical exertion, which may be a syncopal trigger in some (11). Screening of relatives is recommended for anyone suspected of having a swimming-related arrhythmia syndrome. Counseling regarding safe water-related activities and β-blockade therapy are recommended for affected individuals.



The use of alcohol or other intoxicating substances is associated with submersions in older adolescents. Alcohol usage is found in 20% of all submersion injuries in adolescents 15 years and older (38) and in 25%–50% of recreational water deaths in adolescents and adults (31,35). Moreover, the intoxicated victim may vomit, with aspiration of gastric contents. Other medical conditions that less frequently predispose to drowning include depression, coronary artery disease, cardiomyopathy, hypoglycemia, and hypothermia.



Table 28.1 Medical conditions that predispose children to submersion events

Seizure disorder
Long QT syndrome or other “channelopathies”
Use of alcohol or other illicit substances
Other conditions that less frequently predispose to drowning:
   Depression
   Coronary artery disease
   Cardiomyopathy
   Hypoglycemia
   Hypothermia



Submersion injuries in older children and adolescents may be associated with cervical spine injury. The incidence of such injury is low, estimated at 0.5%–5.0% of submersions (24,46). The mechanism of injury is diving or falling into a body of water with a blow that hyperextends the cervical spine. A history of diving is usually elicited (46). When evaluating victims of unwitnessed events, the possibility of associated cervical spine injury should be considered. Immobilization of the cervical spine at the scene is imperative. As with other injuries of the spine, the diagnosis of injury is a clinical one and is based on suspicion about the mechanism of injury and the patient's neurologic condition. Radiographs of the cervical spine may be normal despite debilitating cord injury (41), and MR imaging may be necessary to confirm the clinical suspicion.

P.409




Pathophysiology



The initial sequence of events in drowning was studied during the 1930s, using animals, and consists of the following: initial struggle sometimes with a surprise inhalation, suspension of movement and exhalation of a little air, frequently followed by swallowing, violent struggle, convulsions with spasmodic respiratory efforts through an open mouth, loss of reflexes, and death. This sequence has been confirmed in many cases by bystanders who witness the struggle and subsequent motionlessness. During the initial seconds of submersion, small amounts of fluid are aspirated, often causing laryngospasm. Victims who are resuscitated at this phase will have little water aspiration, but ventilation by rescue breathing may be difficult because of glottic closure. If the victim loses muscle tone, larger quantities of fluid may be aspirated. In addition, a victim may swallow a large amount of fluid and may vomit, aspirating gastric contents.

The development of hypothermia is extremely common with submersion. The presence of hypothermia, in most cases, should not be interpreted as a “cold-water drowning,” a particular situation that will be discussed later. Rather, hypothermia is usually secondary to rapid radiant heat losses in tepid water. As core temperature drops below the mid-30s°C, the victim may develop muscular weakness, and aspiration is facilitated. At lower core temperatures, unconsciousness ensues. Atrial fibrillation occurs with core temperatures in the low 30s°C and ventricular fibrillation or asystole with severe hypothermia (core temperature <28°C) (25,35). Coagulopathy, platelet dysfunction, and immunologic dysfunction also may occur with severe hypothermia.

Fluid and Electrolyte Disturbances



Much has been made of possible fluid shifts and electrolyte disturbances occurring during submersions. Postmortem examination has demonstrated mild-to-moderate hyponatremia of victims who drowned in fresh water and moderate hypernatremia and hyperchloremia in those who drown in salt water. However, clinically important abnormalities in serum electrolyte concentrations usually are not found in patients who survive the event. Exceptions to this generality are found in near-drownings that occur in high-salinity water such as found in the Dead Sea. In addition, hypermagnesemia has been described in seawater drowning, probably a result of both aspiration and ingestion (13). Similarly, important disorders of vascular volume are not often found after drowning. Fresh-water-associated hemodilution and hypervolemia are generally mild. Hypovolemia after saltwater drowning may be seen in severe cases, usually in victims who do not survive.

Respiratory and Cardiovascular Dysfunction



Submersion victims experience some period of hypoxia. For those with brief episodes, hypoxemia is limited to the duration of hypopnea or apnea and may resolve with rescue or initial resuscitation efforts. However, many patients, even those with relatively short-duration hypoxia, may develop increased permeability of pulmonary capillaries, with alveolar fluid leak and dysfunction of surfactant. In patients with longer hypoxic episodes or alveolar aspiration, these processes are more aggressive, with resultant lung collapse, alveolar derecruitment, intrapulmonary shunting, raised pulmonary vascular resistance, and ventilation-perfusion mismatching. Additional cardiac dysfunction may lead to left atrial hypertension and pulmonary-capillary engorgement, furthering pulmonary capillary leak. Large and small airway dysfunction may occur, exacerbating gas exchange problems by trapping gas (29). In combination, these processes create the clinical syndromes of acute lung injury and, later, acute respiratory distress syndrome (ARDS) (26). Aspiration of gastric contents may add caustic injury to airways and alveoli, worsening gas trapping and hypoxemia. Neurogenic pulmonary edema may contribute to deficits in gas exchange and lung function.



The hallmark of cardiovascular dysfunction with submersion injury is shock (33). Systemic and pulmonary vascular resistances are raised with hypothermia and sympathetic activity associated with the diving reflex. With these processes, ventricular end-diastolic pressures are raised, as are atrial pressures, with resultant congestion of central and pulmonary veins. Myocardial contractility is diminished with hypoxemia. Poor myocardial contractility, in combination with raised systemic vascular resistance, results in lower cardiac output. The clinical examination is one of “cold” shock, with poor perfusion and end-organ dysfunction. The degree to which such derangements are reversible with resuscitation efforts is related to the duration of hypoxemia and low-flow states. Important end-organ (kidneys, liver, etc.) dysfunctions may be demonstrable during the patient's hospitalization but usually fully recover with supportive care.



Hypoxic-Ischemic Brain Injury



The most important sequela of submersion injuries is global hypoxic-ischemic brain injury. The combination of hypoxemia and low-flow states results in a host of pathologic processes, including energy failure, lipid peroxidation, production of free radicals, inflammatory responses, and release of excitotoxic neurotransmitters. Disruption of neuronal and glial functions and architecture occurs. Neuronal losses occur with activation of immediate early genes (40) and initial neuronal death, followed days later by so-called “delayed neuronal drop out.” The vascular end zones are particularly vulnerable, and
“watershed” infarctions may be appreciated on CT scans. With a more extensive hypoxic-ischemic insult, a CT scan of the brain may show a “reversal sign” or global “ground glass” appearance, with attenuation of signal in the supratentorial intracranial contents or entire brain, respectively.



Submersion in Ice-Cold Water



While the functional outcome after submersion injury is usually related to the duration and depth of the hypoxic-ischemic insult, brain function may be preserved in cold-water drowning, with good and even normal neurologic outcomes observed despite extensive submersions. Numerous reports have documented dramatic cases of intact neurologic functioning in children who drowned in icy water (6,14,23,44). The term “cold-water drowning” is a misnomer, in that the submersion must occur in ice-cold water and, with very rare exceptions (34), is a phenomenon restricted to northern climates (5). Patients who have drowned in more temperate water but who have become hypothermic should be considered to have hypothermia from prolonged submersion. Such secondary hypothermia is often a poor prognostic sign.



Young children are particularly susceptible to rapid cooling of the brain in icy water because of little subcutaneous fat insulation and a large head-to-body ratio. Moreover, activation of the diving reflex slows metabolism and preserves some perfusion to the heart and brain. Additionally, neurologic preservation can be seen when the lower body is submersed in ice water and the head remains above water, allowing the victim to continue to breathe. The result is rapid brain cooling in the face of residual perfusion and provision of brain substrates.



Table 28.2 Important principles for the management of children with submersion injury

IN THE EMERGENCY DEPARTMENT

Establish adequate oxygenation and ventilation

Intubate airway of unconscious or hypoventilating children
Provide supplemental oxygen

Establish normal circulation

Bolus IV fluids (NS) for hypotension
Initiate use of vasopressor infusions (epinephrine, consider addition of vasopressin) for continued hypotension

Neurologic examination

Determine Glasgow Coma Scale score
Control seizures with bolus administration of anticonvulsants (lorazepam, phenobarbital, or fosphenytoin)

Rewarming of hypothermia, unless mild (35–36°C)

Use warmed fluids and ventilation with heated gas
Consider bladder washes with warmed fluids
Consider cardiopulmonary bypass

Transfer patient for definitive care

Transfer to inpatient unit for observation if full neurologic and cardiovascular function are rapidly restored
Transfer to a PICU if full function not restored





IN THE PICU

Employ ventilator strategies for ALI/ARDS

Limit ventilator peak pressures to <25 torr
Limit tidal volumes to 6–8 mL/kg
Limit fraction of inspired oxygen to <0.60
Liberal use of PEEP
Consider the use of exogenous surfactant or ECMO for continued hypoxemia

Treat myocardial dysfunction

Titrate vasoactive infusions to normal cardiac output and adequate end-organ perfusion

Employ brain-protective strategies

Avoid hyperthermia
Treat clinical and subclinical seizures
Use mild systemic cooling (35–36°C) for 24–48 hrs
Frequent neurologic reassessments and adjunct studies of function as indicated

Refer to a rehabilitation facility for persistent neurologic injury upon recovery

NS, normal saline; ALI, acute lung injury; ARDS, acute respiratory distress syndrome; PEEP, positive end-expiratory pressure; ECMO, extracorporeal membrane oxygenation



Management



Management at the scene should focus on rapid restoration of oxygenation and spontaneous circulation with basic cardiopulmonary resuscitation. Emergency medicine services should be summoned as quickly as possible. No attempts should be made to drain water from the lungs before initiation of rescue breathing. Bystanders should perform mouth-to-mouth breathing even before the victim is removed from the water. Trained rescuers, equipped with a buoyant rescue aid, should attempt in-water rescue breathing of the victim found in deep water (37). Once on solid ground, chest compressions should be performed unless the presence of a pulse is established. As previously discussed, cervical spine immobilization should be performed in cases with a history of diving, or when the cause of drowning is not known. Spinal immobilization is otherwise unnecessary and should not interfere with resuscitative efforts. Advanced life support should be initiated by paramedics for victims who do not regain spontaneous breathing and consciousness with rescue breaths. Bag-valve-mask ventilation with supplemental oxygen is sufficient to restore circulation in some victims. Endotracheal intubation with manual ventilation, administration of fluid boluses, defibrillation, and administration of bolus vasoactive medications (32) may be required in others; however, these efforts should not be pursued to the extent that transportation of the victim to a hospital is delayed.



Management in the Emergency Department



Definitive management of submersion injuries begins in the emergency department. Advanced life support should focus on establishment of adequate oxygenation and ventilation, adequate circulation, and determination of neurologic functioning (Table 28.2). Initial neurologic status is approximated using the Glasgow Coma Scale, a 3–15-point combination score reflecting best verbal, motor, and eye-opening functions in response to graded stimuli. A more thorough neurologic examination is performed later. Repeated Glasgow Coma Scale determinations during the first 12 hrs of treatment and repeated neurologic examinations throughout hospitalization are necessary to document improvement in function. More importantly, frequently repeated examinations may detect deterioration in neurologic condition (e.g., deterioration in neurologic function with the onset of subclinical seizures), which must be evaluated for possible treatable causes.

In the emergency department, definitive warming should be initiated for all but mild hypothermia (35–36°C) and performed in concert with resuscitation efforts. The simplest warming techniques include the use of warmed IV fluids, external radiant heat, ventilation with heated gas, and immersion in a warm bath. More aggressive efforts are necessary for moderate hypothermia: warmed peritoneal lavage or dialysis fluids and/or bladder washes with warm fluids. For severe hypothermia, passive rewarming can induce “rewarming shock,” with peripheral vasodilatation and impaired cardiac output. The use of cardiopulmonary bypass has been advocated for core rewarming in severe hypothermia (44,49). Failure to restore circulation after 30 mins of rewarming to ≥32°C suggests that further resuscitation efforts will not be successful. However, rewarming efforts should not be overly aggressive. Studies of hypothermic treatment in adults with cardiac arrest demonstrate that brain cooling is neuroprotective and that better-than-expected neurologic outcomes are possible (4,21,50). Given this encouraging data, consideration should be given to maintaining mild hypothermia (core temperature of 32–35°C) in children who remain comatose after submersion (47). Certainly, overwarming should be avoided.



Management in the PICU



Children who do not regain full consciousness in the emergency department should be transferred to a pediatric intensive care facility. There, ongoing efforts should be to aggressively treat any cardiorespiratory dysfunction. An “open lung” strategy should be employed for patients with acute lung injury or ARDS. Usual ventilator settings include limiting ventilator peak pressures to 25 torr, tidal volumes to 6–8 mL/kg, and fraction of inspired oxygen to <0.60. Liberal use of positive end-expiratory pressure may improve oxygenation dramatically. Permissive hypercapnia, a commonly used lung-protective strategy, is contraindicated if intracranial hypertension is suspected. Administration of exogenous surfactant was used successfully to treat severe ARDS following submersion injury when surfactant wash out/dysfunction was suspected (36). Extracorporeal membrane oxygenation was used successfully in similar circumstances (17). Continuous vasoactive

infusions may be required to treat myocardial dysfunction and correct abnormal peripheral vascular resistance. Treatment should concentrate on normalizing blood pressure, organ perfusion, and gas exchange as quickly as possible, and frequent repeated examinations are necessary to detect deterioration in cardiorespiratory function.



The other focus of ICU care is restoration of cerebral function, although no definitive treatment exists to reverse the neuronal injury processes previously discussed. Instead, care of the brain is supportive. Normal cardiorespiratory function should be maintained. Hypermetabolic states, such as seizures and fevers, should be aggressively treated. Routine electroencephalography (EEG) should be used to detect subclinical seizures and to titrate antiepileptic therapy. In cases of severe global brain injury, consideration should be given to maintaining mild hypothermia for 24–48 hrs, as previously discussed. To maintain a hypothermic state, patients may require the use of neuromuscular blocking agents, which will interfere with performance of the neurologic examination. In addition, intracranial hypertension may be found in cases of severe brain injury. Despite previous enthusiasm for monitoring and treatment of intracranial pressure, no evidence suggests that such management affects ultimate outcome. Rather, raised intracranial pressure is a marker of poor neurologic prognosis.



Prevention



The outcome of a drowning event is determined in the first few minutes of submersion. As options are available in terms of primary therapy for these injuries, an emphasis on prevention is necessary. Prevention strategies have focused on calling attention to the common causes of childhood drowning, specifically bathtub drowning and recreation-related incidents (48). Slogans such as, “Don't Turn Your Back On Me” alert parents to the proper supervision of infants and toddlers. Other alerts focus on specific events; e.g., the installation of a home pool. Most pool-related submersions occur within the first 6 months of pool exposure (45). The absence of proper pool fencing may increase the odds of pool-related drowning by as much as three- to five-fold (45). Written alerts about drowning risks are generally distributed to customers upon purchase of a new pool.



Additional prevention campaigns have focused on the family pediatrician. The American Academy of Pediatrics issued a policy statement in 2003 to guide pediatricians in incorporating regular, age-appropriate teaching about water safety in their anticipatory guidance to families. Their recommendations can be found at The Injury Prevention Program website, www.aap.org/family/tippmain.htm. Additional prevention tips are available at the Consumer Product Safety Commission website, http://www.cpsc.gov/. Such strategies have met with some success. Reduction in some types of submersions was noted in the UK perhaps due to initiatives on children's safety in water (42).



Outcomes



Outcome from drowning is related to the extent of cerebral injury. However, this outcome is difficult to predict. Poor prognostic signs include an unwitnessed event, prolonged time to resuscitation, the need for cardiopulmonary resuscitation at the scene and in the emergency department (22), and prolonged coma. The best independent predictor of survival is submersion time (39,43); however, in many patients, these data are not known. In Toronto, investigators found the presence of a detectable heartbeat and hypothermia at the initial examination in the emergency department to be discriminate predictors of good outcome versus death or persistent vegetative state (5). However, these findings may not be generalizable; rather, they may reflect the somewhat unique occurrence in Ontario of submersion in frigid water. In the emergency department, a physical examination remarkable for nonreactive pupils or a Glasgow Coma Scale score of ≤5 predict poor neurologic outcome (30); but, these are not absolute predictors.



Specific prognostic scales are similarly less satisfactory in discriminatory function. The Pediatric Risk of Mortality Score (PRISM), a predictor of mortality in critical illness, discriminates between death and the presence or absence of poor outcome, but it is unable to distinguish between different degrees of neurologic dysfunction (20). Other clinical classification systems developed specifically for drowning events have been similarly inadequate (12). A reasonable approach, therefore, is to avoid determining which patients should receive initial treatment based on prognostic factors. Rather, the “treat-them-all approach” applies, with aggressive efforts despite initial lack of heartbeat (30). The adage, “you're not dead until you're warm and dead,” applies with vigorous resuscitative efforts, including rewarming, as needed. Prognosis is deferred until circulation is restored and perfusion optimized. At that time, the patient can be more completely examined.



In those who remain with coma or altered mental status upon restoration of normal circulation, prognosis is usually determined using interim assessments. Repeated clinical neurologic examinations are perhaps the most reliable basis for estimate of outcome. Adjunct studies are often necessary. CT is used in the initial assessment of patients, especially in patients with a history of possible associated traumatic injury. Repeated brain CT scans often add little more information. MRI and MR spectroscopy can detect more subtle injury (16,27). Serial MR scans obtained 3 to 4 days after injury in a series of near-drowning victims admitted to a PICU provided excellent predictive values (16); however, ultimate brain dysfunction has been reported despite normal MR scans (23). Electrophysiologic studies may provide additional information. The early use of electroencephalography may be limited by the need for sedatives in the initial recovery phase, but persistent low attenuation of the electroencephalogram is a poor prognostic sign (28). Brainstem auditory-evoked responses have been used to evaluate function in prolonged outcome with some success (18). Use of a series of electrophysiologic modalities, including sleep recordings, brainstem auditory-evoked responses, somatosensory-evoked potentials, and polysomnography to generate a more complete picture of functioning in 5 comatose children after near-drowning events suggested that better prediction could be attained using all of these modalities over the use of EEG alone (10). No single prognostic test or assessment can reliably discriminate good from poor functional outcomes in all victims of submersion injury; moreover, no indicator is sufficiently reliable to be the sole determinant of whether to withdraw or withhold therapy in a victim of submersion injury.



Conclusions and Future Directions



Submersion injury is one of the leading causes of accident-related mortality and morbidity in childhood. The pathophysiologic processes of such injury are those of hypoxia-ischemia. At present, therapy is focused on restoration of oxygenation and circulation at the scene, with rapid transfer to an emergency department and pediatric intensive care facility when the patient does not experience rapid, full recovery. At present, therapy for brain injury is largely limited to good supportive care and avoidance of secondary insults. The impact of advancements in critical care in the last decade, such as the use of surfactant or inhaled nitric oxide for submersion-related ARDS has not been studied. However, such therapies remain promising and should be considered. Similarly, the use of mild hypothermia early in the PICU course should be considered for submersion victims with neurologic deficits. However, as the central nervous system suffers the most enduring damage in these patients, substantial improvements in outcomes will not be realized until more effective primary therapies for hypoxic-ischemic brain injury are found.



Key Points

Submersion injury is the leading cause of accident related death and disability.

Two age groups are primarily affected: infants and toddlers, and adolescents.

Therapy consists of rapid restoration of respiration and circulation.

Therapy for brain injury includes supportive care and, possibly, mild hypothermia.

No specific prognostic tests or examinations exist.

Prevention of submersion injuries is an important public health goal.



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