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CPR.
Cardiopulmonary Resuscination.
INITIALAPPROACH 1 Cardiopulmonary resuscitation (CPR) is required if a collapsed person is unconscious or unresponsive, not breathing, and has no pulse in a large artery such as the carotid or femoral.
(i) The following may also be seen:
(a) occasional, ineffectual (agonal) gasps
(b) pallor or cyanosis
(c) dilated pupils
(d) brief tonic grand mal seizure.
2 Sudden cardiac arrest still causes over 60% of deaths from coronary heart disease in adults.
Management. 1 This is based on the International Liaison Committee on Resuscitation (ILCOR) 2010 International Consensus on CPR Science with Treatment Recommendations (CoSTR).
(i) The first person on the scene stays with the patient, checks for danger and commences resuscitation, making a note of the time.
(ii) The second person summons help to organize the arrival of equipment, then assists with the resuscitation.
2 Immediate actions
The aim is to maintain oxygenation of the brain and myocardium until a stable cardiac output is achieved.
(i) Lay the patient flat on a hard surface such as a trolley. If the patient is on the floor and enough people are available, lift the
patient onto a trolley to facilitate the resuscitation procedure.
(ii) Rapidly give a single, sharp precordial thump within the first few seconds of the onset of a witnessed or monitored arrest, where the
rhythm is pulseless ventricular tachycardia (VT) or ventricular fibrillation (VF), and a defibrillator is not immediately to hand.
(iii) Check the victim for a response, and then open the airway by tilting the head and lifting the chin if there is no response (‘head
tilt, chin lift’):
(a) this prevents the tongue from occluding the larynx
(b) look, listen and feel for breathing for no more than 10 s, while keeping the airway open.
(iv) If breathing is not normal or absent, check for signs of a circulation:
(a) assess a large pulse such as the carotid or femoral, or look for signs of life for no more than 10 s.
(v) Start CPR immediately if there are no signs of life:
(a) commence external cardiac massage
(b) commence assisted ventilation.
3 External cardiac massage
(i) Place the heel of one hand in the centre of the patient’s chest.Place the heel of the other hand on top, interlocking the fingers.
(ii) Keeping the arms straight and applying a vertical compression force, depress the sternum 5–6 cm at a rate of at least 100
compressions/min (but not exceeding 120/min):
(a) release all the pressure on the chest without losing contact with the sternum after each compression
(b) do not apply pressure over the upper abdomen, lower end of sternum or the ribs, and take equal time for compression and
for release.
(iii) Perform 30 compressions, which should create a palpable femoral pulse.
(iv) Use a one- or two-hand technique to compress the lower half of the sternum in small children by approximately one-third of its
depth, at a rate of at least 100 compressions/min but not greater than 120/min:
(a) use the tips of two fingers in infants, also at a rate of at least 100/min (see p. 343).
4 Assisted ventilation
(i) Open the airway again using head tilt and chin lift.
(ii) Start mouth-to-mouth/nose or mouth-to-mask respiration without delay if breathing is absent, using a pocket mask such as
the Laerdal.
(iii) Deliver two effective rescue breaths that should be completed within 5 s total time, and immediately resume compressions.
(iv) Use a bag-valve mask setup such as an Ambu or Laerdal bag with oxygen reservoir attached and face mask instead, if trained in the
technique
(a) quickly look in the mouth and remove any obstruction with forceps or suction. Leave well-fitting dentures in place
(b) or try inserting an oropharyngeal (Guedel) airway if necessary
(c) check for leaks around the mask or convert to a two-person technique if the chest fails to inflate
(d) consider possible obstruction of the upper airway, if ventilation is still ineffective
CARDIOPULMONARY RESUSCITATION
5 Basic life support: external cardiac massage with assisted ventilation
(i) Continue with chest compressions and rescue breaths in a ratio of 30:2.
(ii) Change the person providing chest compressions every 2 min, but ensure minimum interruption to compressions during the changeover.
6 Defibrillation
(i) As soon as the defibrillator arrives, apply self-adhesive pads or paddles to the patient whilst continuing chest compressions
(a) rapidly shave excessive male chest hair, without delay
(b) place one self-adhesive defibrillation pad or conventional paddle to the right of the sternum below the clavicle, and the
other adhesive pad or paddle in the mid-axillary line level with the V6 electrocardiogram (ECG) electrode or female
breast
(c) avoid positioning self-adhesive pads or paddles over an ECG electrode, medication patch, or implanted device, e.g.
pacemaker or automatic cardioverter defibrillator.
(ii) Analyse the rhythm with a brief pause, and charge the defibrillator if the rhythm is VF or pulseless VT. Continue chest compressions until fully charged.
(iii) Quickly ensure that all rescuers are clear, then give the patient an immediate 150–200 J direct current (DC) shock using a biphasic
waveform defibrillator (all modern defibrillators are now biphasic)
(a) minimize the delay in delivering the shock, which should take less than 5 s
(b) ensure good electrical contact is made when applying manual paddles by using gel pads or electrode jelly, and apply firm
pressure of 8 kg force in adults
(c) give a 360 J shock if an older monophasic defibrillator is used.
(iv) Immediately resume chest compressions without reassessing the rhythm or feeling for a pulse.
(v) The only exception is when VF is witnessed in a patient already connected to a manual defibrillator, or during cardiac
catheterization, and/or early post-cardiac surgery
(a) use a stacked, three-shock strategy rapidly delivering three shocks in a row before starting chest compressions.
(vi) Continue external chest compressions and assisted ventilation for 2 min, then pause briefly to assess the rhythm again.
Warning: adequate oxygenation is achieved by the above measures. Endotracheal intubation should only be attempted by those who are
trained, competent and experienced.
CARDIOPULMONARY RESUSCITATION
7 Observe one of four possible traces
(i) Shockable rhythms such as VF) or pulseless VT
(ii) Non-shockable rhythms such as asystole and pulseless electrical activity (PEA)
8 Establish an initial i.v. line in the antecubital fossa.
(i) Give at least 20 mL of normal saline to flush any drugs administered, that are given after the third DC shock.
(ii) Elevate the limb for 10–20 s to facilitate drug delivery to the central circulation.
(iii) Establish a second i.v. line unless the cardiac resuscitation is rapidly successful
(a) ideally this line should be inserted into a central vein, either the external or internal jugular or the subclavian
(b) a central line should only be inserted by a skilled doctor, as inadvertent arterial puncture, haemothorax or pneumothorax
may invalidate further resuscitation attempts
(c) also, the central venous route poses additional serious hazards should thrombolytic therapy be indicated
(d) all drugs are then given via this central line.
9 Endotracheal intubation
A skilled doctor with airway training may insert a cuffed endotracheal tube This maintains airway patency, prevents regurgitation with
inhalation of vomit or blood from the mouth or stomach, and allows lung ventilation without interrupting chest compressions.
(i) Confirm correct endotracheal tube placement by seeing the tube pass between the vocal cords, and by observing bilateral chest
expansion, and auscultating the lung fields and over the epigastrium.
(ii) Immediately connect an exhaled carbon dioxide detection device such as a waveform capnograph, and look for a tracing, as the
signs above are not completely reliable
(a) never delay CPR to intubate the airway except for a brief pause in chest compressions of not more than 10 s, as the
tube is passed between the vocal cords.
(iii) Once the airway has been secured, continue cardiac compressions uninterrupted at a rate of at least 100/min, and ventilate the lungs
at 10 breaths/min (without any need now to pause for the chest compressions)
(a) take care not to hyperventilate the patient at too fast a rate.
10 Subsequent management depends on the cardiac rhythm and the patient’s condition. Keep the ECG monitor attached to the patient at all time
INITIALAPPROACH 1 Cardiopulmonary resuscitation (CPR) is required if a collapsed person is unconscious or unresponsive, not breathing, and has no pulse in a large artery such as the carotid or femoral.
(i) The following may also be seen:
(a) occasional, ineffectual (agonal) gasps
(b) pallor or cyanosis
(c) dilated pupils
(d) brief tonic grand mal seizure.
2 Sudden cardiac arrest still causes over 60% of deaths from coronary heart disease in adults.
Management. 1 This is based on the International Liaison Committee on Resuscitation (ILCOR) 2010 International Consensus on CPR Science with Treatment Recommendations (CoSTR).
(i) The first person on the scene stays with the patient, checks for danger and commences resuscitation, making a note of the time.
(ii) The second person summons help to organize the arrival of equipment, then assists with the resuscitation.
2 Immediate actions
The aim is to maintain oxygenation of the brain and myocardium until a stable cardiac output is achieved.
(i) Lay the patient flat on a hard surface such as a trolley. If the patient is on the floor and enough people are available, lift the
patient onto a trolley to facilitate the resuscitation procedure.
(ii) Rapidly give a single, sharp precordial thump within the first few seconds of the onset of a witnessed or monitored arrest, where the
rhythm is pulseless ventricular tachycardia (VT) or ventricular fibrillation (VF), and a defibrillator is not immediately to hand.
(iii) Check the victim for a response, and then open the airway by tilting the head and lifting the chin if there is no response (‘head
tilt, chin lift’):
(a) this prevents the tongue from occluding the larynx
(b) look, listen and feel for breathing for no more than 10 s, while keeping the airway open.
(iv) If breathing is not normal or absent, check for signs of a circulation:
(a) assess a large pulse such as the carotid or femoral, or look for signs of life for no more than 10 s.
(v) Start CPR immediately if there are no signs of life:
(a) commence external cardiac massage
(b) commence assisted ventilation.
3 External cardiac massage
(i) Place the heel of one hand in the centre of the patient’s chest.Place the heel of the other hand on top, interlocking the fingers.
(ii) Keeping the arms straight and applying a vertical compression force, depress the sternum 5–6 cm at a rate of at least 100
compressions/min (but not exceeding 120/min):
(a) release all the pressure on the chest without losing contact with the sternum after each compression
(b) do not apply pressure over the upper abdomen, lower end of sternum or the ribs, and take equal time for compression and
for release.
(iii) Perform 30 compressions, which should create a palpable femoral pulse.
(iv) Use a one- or two-hand technique to compress the lower half of the sternum in small children by approximately one-third of its
depth, at a rate of at least 100 compressions/min but not greater than 120/min:
(a) use the tips of two fingers in infants, also at a rate of at least 100/min (see p. 343).
4 Assisted ventilation
(i) Open the airway again using head tilt and chin lift.
(ii) Start mouth-to-mouth/nose or mouth-to-mask respiration without delay if breathing is absent, using a pocket mask such as
the Laerdal.
(iii) Deliver two effective rescue breaths that should be completed within 5 s total time, and immediately resume compressions.
(iv) Use a bag-valve mask setup such as an Ambu or Laerdal bag with oxygen reservoir attached and face mask instead, if trained in the
technique
(a) quickly look in the mouth and remove any obstruction with forceps or suction. Leave well-fitting dentures in place
(b) or try inserting an oropharyngeal (Guedel) airway if necessary
(c) check for leaks around the mask or convert to a two-person technique if the chest fails to inflate
(d) consider possible obstruction of the upper airway, if ventilation is still ineffective
CARDIOPULMONARY RESUSCITATION
5 Basic life support: external cardiac massage with assisted ventilation
(i) Continue with chest compressions and rescue breaths in a ratio of 30:2.
(ii) Change the person providing chest compressions every 2 min, but ensure minimum interruption to compressions during the changeover.
6 Defibrillation
(i) As soon as the defibrillator arrives, apply self-adhesive pads or paddles to the patient whilst continuing chest compressions
(a) rapidly shave excessive male chest hair, without delay
(b) place one self-adhesive defibrillation pad or conventional paddle to the right of the sternum below the clavicle, and the
other adhesive pad or paddle in the mid-axillary line level with the V6 electrocardiogram (ECG) electrode or female
breast
(c) avoid positioning self-adhesive pads or paddles over an ECG electrode, medication patch, or implanted device, e.g.
pacemaker or automatic cardioverter defibrillator.
(ii) Analyse the rhythm with a brief pause, and charge the defibrillator if the rhythm is VF or pulseless VT. Continue chest compressions until fully charged.
(iii) Quickly ensure that all rescuers are clear, then give the patient an immediate 150–200 J direct current (DC) shock using a biphasic
waveform defibrillator (all modern defibrillators are now biphasic)
(a) minimize the delay in delivering the shock, which should take less than 5 s
(b) ensure good electrical contact is made when applying manual paddles by using gel pads or electrode jelly, and apply firm
pressure of 8 kg force in adults
(c) give a 360 J shock if an older monophasic defibrillator is used.
(iv) Immediately resume chest compressions without reassessing the rhythm or feeling for a pulse.
(v) The only exception is when VF is witnessed in a patient already connected to a manual defibrillator, or during cardiac
catheterization, and/or early post-cardiac surgery
(a) use a stacked, three-shock strategy rapidly delivering three shocks in a row before starting chest compressions.
(vi) Continue external chest compressions and assisted ventilation for 2 min, then pause briefly to assess the rhythm again.
Warning: adequate oxygenation is achieved by the above measures. Endotracheal intubation should only be attempted by those who are
trained, competent and experienced.
CARDIOPULMONARY RESUSCITATION
7 Observe one of four possible traces
(i) Shockable rhythms such as VF) or pulseless VT
(ii) Non-shockable rhythms such as asystole and pulseless electrical activity (PEA)
8 Establish an initial i.v. line in the antecubital fossa.
(i) Give at least 20 mL of normal saline to flush any drugs administered, that are given after the third DC shock.
(ii) Elevate the limb for 10–20 s to facilitate drug delivery to the central circulation.
(iii) Establish a second i.v. line unless the cardiac resuscitation is rapidly successful
(a) ideally this line should be inserted into a central vein, either the external or internal jugular or the subclavian
(b) a central line should only be inserted by a skilled doctor, as inadvertent arterial puncture, haemothorax or pneumothorax
may invalidate further resuscitation attempts
(c) also, the central venous route poses additional serious hazards should thrombolytic therapy be indicated
(d) all drugs are then given via this central line.
9 Endotracheal intubation
A skilled doctor with airway training may insert a cuffed endotracheal tube This maintains airway patency, prevents regurgitation with
inhalation of vomit or blood from the mouth or stomach, and allows lung ventilation without interrupting chest compressions.
(i) Confirm correct endotracheal tube placement by seeing the tube pass between the vocal cords, and by observing bilateral chest
expansion, and auscultating the lung fields and over the epigastrium.
(ii) Immediately connect an exhaled carbon dioxide detection device such as a waveform capnograph, and look for a tracing, as the
signs above are not completely reliable
(a) never delay CPR to intubate the airway except for a brief pause in chest compressions of not more than 10 s, as the
tube is passed between the vocal cords.
(iii) Once the airway has been secured, continue cardiac compressions uninterrupted at a rate of at least 100/min, and ventilate the lungs
at 10 breaths/min (without any need now to pause for the chest compressions)
(a) take care not to hyperventilate the patient at too fast a rate.
10 Subsequent management depends on the cardiac rhythm and the patient’s condition. Keep the ECG monitor attached to the patient at all time
Tag :
CPR,
Sore throat.Sore throat in a 29-year-old male.
Sore throat in a 29-year-old male.
HISTORY OF PRESENT ILLNESSA 29-year-old male with a medical history significant for type I diabetes presented to the ED complaining of a sore throat,inability to swallow solids and fevers to 103◦F (39.4◦C) for two days. He noted a hoarse voice and was able to tolerate only small sips of liquids. He denied significant neck swelling or stiffness, and was able to tolerate his secretions. He had immigrated
to the United States from Mexico as a teenager, and his immunization status was unknown.
PHYSICAL EXAM
GENERAL APPEARANCE: The patient was a well-developed,nontoxic, moderately obese male who appeared slightly dehydrated,sitting upright and in no acute distress.
VITAL SIGNS
Temperature 103◦F (39.4◦C) ,Pulse 100 beats/minute,Blood pressure 145/85 mmHg,Respirations 22 breaths/minute,Oxygen saturation 100% on room air.
HEENT(HEAD, EYES, EARS,NOSE AND THROAT): Oropharynx was pink and moist, no erythema, exudates,tonsillar or uvular swelling noted.
NECK: Supple, anterior cervical lymphadenopathy noted, tenderness to palpation over cricoid cartilage noted.
LUNGS: Clear to auscultation bilaterally.
CARDIOVASCULAR: Regular rate and rhythm without rubs,murmurs or gallops.
ABDOMEN: Soft, nontender, nondistended.
EXTREMITIES: No clubbing, cyanosis or edema.
A peripheral intravenous line was placed and blood wasdrawn and sent for laboratory testing. Laboratory tests were significant for a leukocyte count of 24 K/μL (normal 3.5–12.5 K/μL) with 92% neutrophils (normal 50–70%). A softtissue lateral neck radiograph was obtained (Figure 1.1).
What is your diagnosis?ANSWER .The diagnosis is epiglottitis. The soft-tissue lateral neck radiograph demonstrates swelling of the epiglottis (“thumbprint” sign, Figure 1.2). The Ear, Nose and Throat (ENT) specialist was urgently consulted,and bedside nasopharyngoscopy demonstrated a swollen, red epiglottis with 90% obstruction of the upper airway. The patient received ceftriaxone 1 gm and decadron 10 mg intravenously, normal saline 1 liter IV bolus,and was admitted to the ICU for close monitoring and observation.The patient was discharged on hospital day #4 after his
symptoms had improved. Repeat nasopharyngoscopy demonstrated significant improvement of the epiglottic swelling. He was continued on cefpodoxime proxetil (VantinTM) orally for ten days following discharge.
Epiglottitis in adults.
Acute epiglottitis is a potentially life-threatening condition that results from inflammation of the supraglottic structures.1,2 Commonly considered a pediatric disease,thecurrent incidence of epiglottitis in adults is 1 to 2 cases per 100,000, which is presently 2.5 times the incidence in
children.1 Epiglottitis occurs most frequently in men in the fifth decade; the disease is more common in countries that do not immunize against Haemophilus influenzae type B. Currently,the most common cause of epiglottitis is infection,although sources such as crack cocaine use have also been
implicated.1 Common pathogens include H. influenzae (Hib),β-hemolytic streptococci and viruses.
The clinical presentation of adult epiglottitis may differ significantly from that of the classic drooling child seated in a tripod position. The most common symptoms in adults are sore throat, odynophagia and muffled voice.3 Sore throat is the chief complaint in 75–94% of cases, whereas odynophagia
may be present in as many as 94% of cases.4 The presence of stridor significantly increases the need for emergent airway intervention.5 Unlike children with epiglottitis, where emergency airway management is essential, most cases of adult epiglottitis do not require acute airway intervention due
to the greater diameter of the adult airway.The leukocyte count is greater than 10,000 in 80% of
cases of adult epiglottitis. Soft-tissue lateral neck radiography,which may show an enlarged, misshapen epiglottis(“thumbprint” sign), has a sensitivity of 88% in establishing the diagnosis.3 Patients who appear ill or are in extremis should not leave the ED for radiographs, and airway management in patients in extremis should be the first and foremost responsibility. Direct laryngoscopy is the most accurate investigation to establish a diagnosis of epiglottitis.3 Management
focuses on two important aspects: close monitoring of the airway with intubation (if necessary) and treatment with intravenous antibiotics.6 Antibiotics should be directed against Hib in every patient, regardless of immunization status. Cefotaxime,ceftriaxone or ampicillin/sulbactam are appropriate choices. Steroids are commonly used in the management of
KEY TEACHING POINTS
1. Acute epiglottitis is a potentially life-threatening condition resulting from inflammation of the supraglottic structures,with a current incidence of 1 to 2 cases per 100,000 adults in the United States.
2. Sore throat is the chief complaint in 75–94% of cases of adult epiglottitis, whereas odynophagia may be present in as many as 94% of cases.
3. Soft-tissue lateral neck radiography, which may show an enlarged, misshapen epiglottis (“thumbprint” sign), has a sensitivity of 88% in establishing the diagnosis.
4. The definitive diagnosis is made through direct laryngoscopic visualization of an enlarged, inflamed epiglottis.
5. Treatment of epiglottitis includes intravenous antibiotics and close airway monitoring in an ICU setting. Most clinicians treat acute cases with intravenous steroids.
HISTORY OF PRESENT ILLNESSA 29-year-old male with a medical history significant for type I diabetes presented to the ED complaining of a sore throat,inability to swallow solids and fevers to 103◦F (39.4◦C) for two days. He noted a hoarse voice and was able to tolerate only small sips of liquids. He denied significant neck swelling or stiffness, and was able to tolerate his secretions. He had immigrated
to the United States from Mexico as a teenager, and his immunization status was unknown.
PHYSICAL EXAM
GENERAL APPEARANCE: The patient was a well-developed,nontoxic, moderately obese male who appeared slightly dehydrated,sitting upright and in no acute distress.
VITAL SIGNS
Temperature 103◦F (39.4◦C) ,Pulse 100 beats/minute,Blood pressure 145/85 mmHg,Respirations 22 breaths/minute,Oxygen saturation 100% on room air.
HEENT(HEAD, EYES, EARS,NOSE AND THROAT): Oropharynx was pink and moist, no erythema, exudates,tonsillar or uvular swelling noted.
NECK: Supple, anterior cervical lymphadenopathy noted, tenderness to palpation over cricoid cartilage noted.
LUNGS: Clear to auscultation bilaterally.
CARDIOVASCULAR: Regular rate and rhythm without rubs,murmurs or gallops.
ABDOMEN: Soft, nontender, nondistended.
EXTREMITIES: No clubbing, cyanosis or edema.
A peripheral intravenous line was placed and blood wasdrawn and sent for laboratory testing. Laboratory tests were significant for a leukocyte count of 24 K/μL (normal 3.5–12.5 K/μL) with 92% neutrophils (normal 50–70%). A softtissue lateral neck radiograph was obtained (Figure 1.1).
What is your diagnosis?ANSWER .The diagnosis is epiglottitis. The soft-tissue lateral neck radiograph demonstrates swelling of the epiglottis (“thumbprint” sign, Figure 1.2). The Ear, Nose and Throat (ENT) specialist was urgently consulted,and bedside nasopharyngoscopy demonstrated a swollen, red epiglottis with 90% obstruction of the upper airway. The patient received ceftriaxone 1 gm and decadron 10 mg intravenously, normal saline 1 liter IV bolus,and was admitted to the ICU for close monitoring and observation.The patient was discharged on hospital day #4 after his
symptoms had improved. Repeat nasopharyngoscopy demonstrated significant improvement of the epiglottic swelling. He was continued on cefpodoxime proxetil (VantinTM) orally for ten days following discharge.
Epiglottitis in adults.
Acute epiglottitis is a potentially life-threatening condition that results from inflammation of the supraglottic structures.1,2 Commonly considered a pediatric disease,thecurrent incidence of epiglottitis in adults is 1 to 2 cases per 100,000, which is presently 2.5 times the incidence in
children.1 Epiglottitis occurs most frequently in men in the fifth decade; the disease is more common in countries that do not immunize against Haemophilus influenzae type B. Currently,the most common cause of epiglottitis is infection,although sources such as crack cocaine use have also been
implicated.1 Common pathogens include H. influenzae (Hib),β-hemolytic streptococci and viruses.
The clinical presentation of adult epiglottitis may differ significantly from that of the classic drooling child seated in a tripod position. The most common symptoms in adults are sore throat, odynophagia and muffled voice.3 Sore throat is the chief complaint in 75–94% of cases, whereas odynophagia
may be present in as many as 94% of cases.4 The presence of stridor significantly increases the need for emergent airway intervention.5 Unlike children with epiglottitis, where emergency airway management is essential, most cases of adult epiglottitis do not require acute airway intervention due
to the greater diameter of the adult airway.The leukocyte count is greater than 10,000 in 80% of
cases of adult epiglottitis. Soft-tissue lateral neck radiography,which may show an enlarged, misshapen epiglottis(“thumbprint” sign), has a sensitivity of 88% in establishing the diagnosis.3 Patients who appear ill or are in extremis should not leave the ED for radiographs, and airway management in patients in extremis should be the first and foremost responsibility. Direct laryngoscopy is the most accurate investigation to establish a diagnosis of epiglottitis.3 Management
focuses on two important aspects: close monitoring of the airway with intubation (if necessary) and treatment with intravenous antibiotics.6 Antibiotics should be directed against Hib in every patient, regardless of immunization status. Cefotaxime,ceftriaxone or ampicillin/sulbactam are appropriate choices. Steroids are commonly used in the management of
KEY TEACHING POINTS
1. Acute epiglottitis is a potentially life-threatening condition resulting from inflammation of the supraglottic structures,with a current incidence of 1 to 2 cases per 100,000 adults in the United States.
2. Sore throat is the chief complaint in 75–94% of cases of adult epiglottitis, whereas odynophagia may be present in as many as 94% of cases.
3. Soft-tissue lateral neck radiography, which may show an enlarged, misshapen epiglottis (“thumbprint” sign), has a sensitivity of 88% in establishing the diagnosis.
4. The definitive diagnosis is made through direct laryngoscopic visualization of an enlarged, inflamed epiglottis.
5. Treatment of epiglottitis includes intravenous antibiotics and close airway monitoring in an ICU setting. Most clinicians treat acute cases with intravenous steroids.
Tag :
epiglottitis,
Sore Throat,
Flu,Cold ,Cough.
.Common Cold Among the acute respiratory illness two-thirds to threefourths are caused by viruses. Most of these viral infections affect the upper respiratory tract, but lower respiratory tract can be involved in certain groups particularly in young age group and in certain epidemiological settings. The illness caused by respiratory viruses expressed into multiple distinct syndromes, such as common cold, pharyngitis, croup, tracheobronchitis, bronchiolitis, pneumonia, etc.Almost everybody suffers from common cold sometime in his life. It occurs more in winter and in cold climates. It is an acute infection of the respiratory tract characterized by sneezing, running nose, nasopharyngeal irritation and malaise lasting two to seven days. Fever is rare. The infectious agent is a rhinovirus with more than 100 serotypes. The patient is highly infective 24 hours preceding and five days following the onset of the disease. Transmission is by droplet method or through fomites such as handkerchief. Susceptibility is general. Immunity is shortlived and lasts for a month or so. Incubation period is
12 to 72 (usually 24) hours.There is no specific treatment. Cold vaccines have been used but the results are not encouraging.
Influenza. Influenza is an acute infectious respiratory disease caused by RNA viruses of the family orthomyxoviridae (the influenza viruses). The influenza virus, known to be circulating as a human pathogen since at least the 16th century is notable for its unique ability to cause recurrent epidemics and global pandemics. Genetic reassortments in the influenza virus cause fast and unpredictable antigenic changes in important immune targets leading to recurrent epidemics of febrile respiratory disease every one to three years. Each century has seen some pandemics rapidly progressing to all parts of the world due to emergence of a novel virus to which the overall population holds no immunity.
CLINICAL FEATURES(Symptoms).
Infection with influenza may be asymptomatic but usually gives rise to fever and typical prostrating disease, characteristic in epidemics. Usual symptoms are flushed
face, congested conjunctivae, cough, sore throat, fever for two to three days, headache, myalgia, back pains and marked weakness. Pneumonia due to secondary bacterial infection is the most common complication. Laboratory confirmation is made by recovery of virus from throat washings or by demonstration of significant rise of influenza antibodies in the serum in acute and convalescent stages of the disease or by direct identification of the virus in nasopharyngeal cells.
EPIDEMIOLOGY
A large number of cases are either missed or are unreported because of their mildness. Hence exact incidence cannot be assessed. Morbidity rate varies from 15 to 25 percent of the population exposed to risk in case of large communities. The rate may be as high as 40 percent in case of closed populations.1 Once an epidemic starts, its peak is reached in three to four weeks before declining.2
The disease was first recognized in 1173; since then 80 epidemics have occurred. The epidemic lasts for six to eight weeks at a place. It is not known what happens to the virus between the epidemics.3 However, there is evidence that transmission of the virus to extrahuman reservoirs (pigs, horses, birds, ducks) keeps the virus cycle alive.4
Immunity: The antibody to H type of antigen prevents initiation of the infection while that to N antigen prevents virus release and spread. The antibodies developed in the respiratory tract following an infection are mostly IgA. They appear in about seven days after an attack and peak in the blood by two weeks. The level drops to preinfection level by 8 to 12 months.Antibody against one influenza virus type or subtype confers limited or no protection against another type or subtype of influenza. Furthermore, antibody to one antigenic variant of influenza virus might not completely protect against a new antigenic variant of the same type or subtype. Frequent development of antigenic variants through antigenic drift is the virologic basis for seasonal epidemics and the reason for the usual incorporation of one or more new strains in each year’s influenza vaccine.
MODE OF TRANSMISSION
Influenza viruses predominantly transmitted through respiratory droplets of coughs and sneezes from an infected person. Influenza viruses may also spread through direct (skin to skin) or indirect contact with infected material, which ultimately enter through nasopharyngeal route. Transmission of viruses starts one day before the onset of symptoms and continue up to five to seven days after the symptoms subsides. Transmission is possible from asymptomatic carriers. Children may pass the virus for
longer than seven days. Influenza viruses can be inactivated by sunlight, disinfectants and detergents easily. Frequent hand washing reduces the risk of infection.
Incubation Period
The incubation time for influenza ranges from one to five days with an average of two days.
Diagnosis
Traditionally, the definitive diagnosis of influenza is made either on the basis of virus isolation or by serology. Virus is most frequently isolated from nasopharyngeal or throat swabs, nasal washings or sputum obtained within three days of onset of illness. Number of tests can help in confirming the diagnosis of influenza. During an outbreak of respiratory illness, however, testing can be very helpful in determining if influenza is the cause of the outbreak. Following laboratory tests that can be
carried out are:
• Detection of antigen in nasal secretions by: – Rapid test: It can be used to detect influenzaviruses within 30 minutes.
– Immunofluorescence test
– Antigen capture ELISA with monoclonal antibody to the nucleoprotein
– Reverse Transcriptase Polymerase Chain Reaction (RT-PCR)
• Virus isolation:
– Cell line Madin-Darby Canine Kidneycells
(MDCK)
– Egg inoculation
• Serological test in paired serum samples
Treatment: 1. Antibiotics for bacterial complications of influenza 2. Antiviral therapy 3. Management of contacts may include-antiviral prophylaxis and advice about relevant vaccination (e.g. pandemic strain vaccine if available) Prevention and control strategies: People with respiratory infection symptoms should practice the following respiratory etiquette. All symptomatic people should: 1. Avoid close contact (less than 1 meter) with other people. 2. Cover their nose and mouth when coughing or sneezing. 3. Use disposable tissues to contain respiratory secretions. 4. Immediately dispose off used tissues.
RECOMMENDED DRUGS AND DOSAGE FOR PROPHYLAXIS OF INFLUENZA
• Amantadine 5 mg/kg/day up 5 mg/kg/day
• Rimantadine
• Oseltamivir
• Zanamivir
12 to 72 (usually 24) hours.There is no specific treatment. Cold vaccines have been used but the results are not encouraging.
CLINICAL FEATURES(Symptoms).
Infection with influenza may be asymptomatic but usually gives rise to fever and typical prostrating disease, characteristic in epidemics. Usual symptoms are flushed
face, congested conjunctivae, cough, sore throat, fever for two to three days, headache, myalgia, back pains and marked weakness. Pneumonia due to secondary bacterial infection is the most common complication. Laboratory confirmation is made by recovery of virus from throat washings or by demonstration of significant rise of influenza antibodies in the serum in acute and convalescent stages of the disease or by direct identification of the virus in nasopharyngeal cells.
EPIDEMIOLOGY
A large number of cases are either missed or are unreported because of their mildness. Hence exact incidence cannot be assessed. Morbidity rate varies from 15 to 25 percent of the population exposed to risk in case of large communities. The rate may be as high as 40 percent in case of closed populations.1 Once an epidemic starts, its peak is reached in three to four weeks before declining.2
The disease was first recognized in 1173; since then 80 epidemics have occurred. The epidemic lasts for six to eight weeks at a place. It is not known what happens to the virus between the epidemics.3 However, there is evidence that transmission of the virus to extrahuman reservoirs (pigs, horses, birds, ducks) keeps the virus cycle alive.4
Immunity: The antibody to H type of antigen prevents initiation of the infection while that to N antigen prevents virus release and spread. The antibodies developed in the respiratory tract following an infection are mostly IgA. They appear in about seven days after an attack and peak in the blood by two weeks. The level drops to preinfection level by 8 to 12 months.Antibody against one influenza virus type or subtype confers limited or no protection against another type or subtype of influenza. Furthermore, antibody to one antigenic variant of influenza virus might not completely protect against a new antigenic variant of the same type or subtype. Frequent development of antigenic variants through antigenic drift is the virologic basis for seasonal epidemics and the reason for the usual incorporation of one or more new strains in each year’s influenza vaccine.
MODE OF TRANSMISSION
Influenza viruses predominantly transmitted through respiratory droplets of coughs and sneezes from an infected person. Influenza viruses may also spread through direct (skin to skin) or indirect contact with infected material, which ultimately enter through nasopharyngeal route. Transmission of viruses starts one day before the onset of symptoms and continue up to five to seven days after the symptoms subsides. Transmission is possible from asymptomatic carriers. Children may pass the virus for
longer than seven days. Influenza viruses can be inactivated by sunlight, disinfectants and detergents easily. Frequent hand washing reduces the risk of infection.
Incubation Period
The incubation time for influenza ranges from one to five days with an average of two days.
Diagnosis
Traditionally, the definitive diagnosis of influenza is made either on the basis of virus isolation or by serology. Virus is most frequently isolated from nasopharyngeal or throat swabs, nasal washings or sputum obtained within three days of onset of illness. Number of tests can help in confirming the diagnosis of influenza. During an outbreak of respiratory illness, however, testing can be very helpful in determining if influenza is the cause of the outbreak. Following laboratory tests that can be
carried out are:
• Detection of antigen in nasal secretions by: – Rapid test: It can be used to detect influenzaviruses within 30 minutes.
– Immunofluorescence test
– Antigen capture ELISA with monoclonal antibody to the nucleoprotein
– Reverse Transcriptase Polymerase Chain Reaction (RT-PCR)
• Virus isolation:
– Cell line Madin-Darby Canine Kidneycells
(MDCK)
– Egg inoculation
• Serological test in paired serum samples
Treatment: 1. Antibiotics for bacterial complications of influenza 2. Antiviral therapy 3. Management of contacts may include-antiviral prophylaxis and advice about relevant vaccination (e.g. pandemic strain vaccine if available) Prevention and control strategies: People with respiratory infection symptoms should practice the following respiratory etiquette. All symptomatic people should: 1. Avoid close contact (less than 1 meter) with other people. 2. Cover their nose and mouth when coughing or sneezing. 3. Use disposable tissues to contain respiratory secretions. 4. Immediately dispose off used tissues.
RECOMMENDED DRUGS AND DOSAGE FOR PROPHYLAXIS OF INFLUENZA
• Amantadine 5 mg/kg/day up 5 mg/kg/day
• Rimantadine
• Oseltamivir
• Zanamivir
Tag :
Common cold,
Hepatitis a
Hepatitis A is a liver disease caused by the hepatitis A virus. The virus is primarily spread when an uninfected (and unvaccinated) person ingests food or water that is contaminated with the faeces of an infected person. The disease is closely associated with unsafe water or food, inadequate sanitation and poor personal hygiene.
Infectious agent
Hepatitis A virus (HAV) is the causative agent.
Symptoms
Illness due to hepatitis A typically causes acute fever, malaise, anorexia, nausea and abdominal discomfort. This is followed a few days later by dark urine and jaundice. Symptoms usually last several weeks although convalescence may sometimes be prolonged. Severe illness may rarely occur when hepatitis A infection complicates pre-existing liver disease. Infants and young children infected with HAV may have a mild
illness with few or no symptoms, with jaundice often being absent.
Method of diagnosis
A blood test indicating IgM anti-HAV antibodies confirms recent infection.These antibodies are present for two to
four months after infection. IgG antibodies alone are evidence of past
infection. In the acute stage of the illness, blood biochemistry shows elevated
transaminase levels indicating hepatocellular damage. The pattern of liver function tests may be non-specific
in later illness.
Incubation period
The incubation period is fifteen to fifty days, with an average of 28–30 days. Public health significance and occurrence Hepatitis A occurs worldwide. In developing countries most people are infected during childhood. With good sanitation and hygiene in the developed world, most people now reach adulthood without experiencing infection. There are about 70–200 cases per year in Victoria. Notifications have been declining nationally since the late 1990s. Infection is more common in travelers to endemic areas, injecting drug users, children in childcare and men who have sex with men. Common source outbreaks due to contaminated food are rare.
Reservoir
Humans.
Mode of transmission
Infection is transmitted by the faecal-oral route from person to person or via fomites. Infectious food handlers may
contaminate non-cooked foods such as salads. Infection can also occur through ingestion of contaminated food or water.Filter-feeding shellfish such as oysters raised in contaminated waters may harbour the virus.The precise timing and mode of transmission are often difficult to define.
Period of communicability
Cases are most infectious from the latter half of the incubation period until a few days after the onset of jaundice,corresponding to a peak in transaminase levels in cases without jaundice. Most
cases are not infectious after the first week of jaundice. Long term carriage or excretion of the virus does not occur.
Susceptibility and resistance
All non immune people are susceptible to infection. Immunity after infection is
probably lifelong. Control measures
Preventive measures
Education about good hygiene is important, particularly hand washing before handling food and eating and after
using the toilet. Inadequate sanitation and housing may contribute to endemic illness.Inactivated hepatitis A vaccines are available for use in persons two years of age and over. Protection begins within
14–21 days after the first dose. A second dose is required for long term protection.The vaccine is recommended for travellers to high risk areas, persons in high risk occupations such as childcare workers and emergency services personnel, injecting drug users and men who have sex with men.
Control of case
Treatment is generally supportive.Exclude from childcare, school or work for at least one week after the onset of
illness or jaundice and until they are well.Children must have a medical certificate
of recovery before returning to school or
child care.
Educate the patient and their family on the need for strict hygiene practices.
Infected persons should not prepare meals for others while infectious, nor share utensils, toothbrushes, towels and face washers.
Dispose of or thoroughly wash nappies of infants that have hepatitis A.
Control of contacts
Normal immunoglobulin (IG) 0.02 mL/kg body weight intramuscularly is recommended for:
• household and sexual contacts of the case
• staff and children in close contact with a case in a childcare centre.
IG is not recommended for usual office, school or factory contacts. IG must be given within seven to ten days of
exposure to be effective. IG is rarely given to persons exposed to a potential common source of hepatitis A such as food or water because cases related to such a source are usually recognised too long after the exposure for IG to be effective. Timely administration of IG will prevent or modify clinical illness for approximately six weeks after the dose. However, people exposed and infected before the administration of IG may still experience a mild infection, and may have the potential to infect others if strict personal hygiene is not maintained. Surveillance of contacts in a household or workplace should be maintained. Live vaccines such as Measles Mumps Rubella (MMR) should not be administered for three months after a dose of IG, and may also be ineffective if given in the 14 days prior to IG. Reschedule such routine vaccinations. When the case is a food handler:
• consider serological testing of coworkers to determine whether they have been infected or are susceptible
• place uninfected susceptible coworkers under surveillance and give them IG prophylaxis. These persons remain at a risk of developing mild illness modified by IG but can generally continue to work provided good personal hygiene and food handling practices are maintained
• undertake surveillance for hepatitis A in patrons by seeking a history of exposure to the food premises from
cases notified over the next two to three months
• carefully consider the role of the infected food handler. If transmission to patrons appears likely, consider urgent
follow-up of exposed patrons to offer them IG prophylaxis.Note that when the index case is a patron, it is usually
too late to offer IG prophylaxis to other diners, although personal contacts of the patron case should be offered IG
according to the usual protocol.When the case is a health care worker,the role of the case should be assessed
and consideration given to the provision of IG prophylaxis for co-workers and patients in their direct care whilst
infectious. Surveillance of contacts in the health care facility should be maintained.
Control of environment
A source of infection should always be sought. For apparently sporadic cases,consider contact with another known case and recent travel to an area where the disease is endemic. Acquisition of infection from young children, particularly those in childcare should be considered. Special attention should be given to toilet hygiene in schools and childcare centres. Ensure that soap and water are available and are used regularly to wash
hands.Food premises, health care facilities or child care centres where a case has worked whilst potentially infective should be requested to carry out a clean up in accordance with the Department’s Guidelines for the investigation of gastrointestinal illness.
Infectious agent
Hepatitis A virus (HAV) is the causative agent.
Symptoms
Illness due to hepatitis A typically causes acute fever, malaise, anorexia, nausea and abdominal discomfort. This is followed a few days later by dark urine and jaundice. Symptoms usually last several weeks although convalescence may sometimes be prolonged. Severe illness may rarely occur when hepatitis A infection complicates pre-existing liver disease. Infants and young children infected with HAV may have a mild
illness with few or no symptoms, with jaundice often being absent.
Method of diagnosis
A blood test indicating IgM anti-HAV antibodies confirms recent infection.These antibodies are present for two to
four months after infection. IgG antibodies alone are evidence of past
infection. In the acute stage of the illness, blood biochemistry shows elevated
transaminase levels indicating hepatocellular damage. The pattern of liver function tests may be non-specific
in later illness.
Incubation period
The incubation period is fifteen to fifty days, with an average of 28–30 days. Public health significance and occurrence Hepatitis A occurs worldwide. In developing countries most people are infected during childhood. With good sanitation and hygiene in the developed world, most people now reach adulthood without experiencing infection. There are about 70–200 cases per year in Victoria. Notifications have been declining nationally since the late 1990s. Infection is more common in travelers to endemic areas, injecting drug users, children in childcare and men who have sex with men. Common source outbreaks due to contaminated food are rare.
Reservoir
Humans.
Mode of transmission
Infection is transmitted by the faecal-oral route from person to person or via fomites. Infectious food handlers may
contaminate non-cooked foods such as salads. Infection can also occur through ingestion of contaminated food or water.Filter-feeding shellfish such as oysters raised in contaminated waters may harbour the virus.The precise timing and mode of transmission are often difficult to define.
Period of communicability
Cases are most infectious from the latter half of the incubation period until a few days after the onset of jaundice,corresponding to a peak in transaminase levels in cases without jaundice. Most
cases are not infectious after the first week of jaundice. Long term carriage or excretion of the virus does not occur.
Susceptibility and resistance
All non immune people are susceptible to infection. Immunity after infection is
probably lifelong. Control measures
Preventive measures
Education about good hygiene is important, particularly hand washing before handling food and eating and after
using the toilet. Inadequate sanitation and housing may contribute to endemic illness.Inactivated hepatitis A vaccines are available for use in persons two years of age and over. Protection begins within
14–21 days after the first dose. A second dose is required for long term protection.The vaccine is recommended for travellers to high risk areas, persons in high risk occupations such as childcare workers and emergency services personnel, injecting drug users and men who have sex with men.
Control of case
Treatment is generally supportive.Exclude from childcare, school or work for at least one week after the onset of
illness or jaundice and until they are well.Children must have a medical certificate
of recovery before returning to school or
child care.
Educate the patient and their family on the need for strict hygiene practices.
Infected persons should not prepare meals for others while infectious, nor share utensils, toothbrushes, towels and face washers.
Dispose of or thoroughly wash nappies of infants that have hepatitis A.
Control of contacts
Normal immunoglobulin (IG) 0.02 mL/kg body weight intramuscularly is recommended for:
• household and sexual contacts of the case
• staff and children in close contact with a case in a childcare centre.
IG is not recommended for usual office, school or factory contacts. IG must be given within seven to ten days of
exposure to be effective. IG is rarely given to persons exposed to a potential common source of hepatitis A such as food or water because cases related to such a source are usually recognised too long after the exposure for IG to be effective. Timely administration of IG will prevent or modify clinical illness for approximately six weeks after the dose. However, people exposed and infected before the administration of IG may still experience a mild infection, and may have the potential to infect others if strict personal hygiene is not maintained. Surveillance of contacts in a household or workplace should be maintained. Live vaccines such as Measles Mumps Rubella (MMR) should not be administered for three months after a dose of IG, and may also be ineffective if given in the 14 days prior to IG. Reschedule such routine vaccinations. When the case is a food handler:
• consider serological testing of coworkers to determine whether they have been infected or are susceptible
• place uninfected susceptible coworkers under surveillance and give them IG prophylaxis. These persons remain at a risk of developing mild illness modified by IG but can generally continue to work provided good personal hygiene and food handling practices are maintained
• undertake surveillance for hepatitis A in patrons by seeking a history of exposure to the food premises from
cases notified over the next two to three months
• carefully consider the role of the infected food handler. If transmission to patrons appears likely, consider urgent
follow-up of exposed patrons to offer them IG prophylaxis.Note that when the index case is a patron, it is usually
too late to offer IG prophylaxis to other diners, although personal contacts of the patron case should be offered IG
according to the usual protocol.When the case is a health care worker,the role of the case should be assessed
and consideration given to the provision of IG prophylaxis for co-workers and patients in their direct care whilst
infectious. Surveillance of contacts in the health care facility should be maintained.
Control of environment
A source of infection should always be sought. For apparently sporadic cases,consider contact with another known case and recent travel to an area where the disease is endemic. Acquisition of infection from young children, particularly those in childcare should be considered. Special attention should be given to toilet hygiene in schools and childcare centres. Ensure that soap and water are available and are used regularly to wash
hands.Food premises, health care facilities or child care centres where a case has worked whilst potentially infective should be requested to carry out a clean up in accordance with the Department’s Guidelines for the investigation of gastrointestinal illness.
Treatment
There is no specific treatment for hepatitis A. Recovery from symptoms following infection may be slow and may take several weeks or months. Most important is the avoidance of unnecessary medications. Acetaminophen / Paracetamol and medication against vomiting should not be given.Hospitalization is unnecessary in the absence of acute liver failure. Therapy is aimed at maintaining comfort and adequate nutritional balance, including replacement of fluids that are lost from vomiting and diarrhoea.
Infectious Diarrhea. Causes,symptoms,Diarrhea treatment.
Diarrhea. An increased frequency of defecation due to a microbial pathogen and defined as greater than 3 stools per day or greater than 200 g of stool per day.
B. Epidemiology
1. Infectious diarrhea is the most common cause of diarrhea worldwide.
2. The second most common cause of death worldwide but the leading cause of childhood death worldwide.
3. In the United States, most episodes occur during the winter months and are due to viral pathogens (eg, noroviruses, rotaviruses).
C. D iarrhea Syndromes
1. Acute infectious diarrhea. Lasting less than 14 days.
a. Acute watery diarrhea without blood
b. Acute dysentery (diarrhea with blood)
2. Chronic or persistent diarrhea. Lasting more than 14 days.
D. Pathogenesis. Pathogens are transmitted through contaminated water or foods/food products and reach the gastrointestinal tract to cause:
1. Increased intestinal secretion of fluid and electrolytes, most commonly in the small intestine, through the production of enterotoxins (eg,cholera toxin, Escherichia coli heat labile and heat stable toxins) that may mediate secretagogues (eg, 5-hydroxytryptamine [5-HT]).
2. Decreased intestinal absorption of fluid and electrolytes in the small and large intestine through intestinal mucosal damage. Severe villous atrophy can occur with infection due to Giardia, Cryptosporidium, Cyclospora, and Microsporidium (intestinal protozoa). An alternative cause of villous atrophy is celiac disease (an autoimmune disorder due to gluten intolerance).
CAUSES OF INFECTIOUS DIARRHEA.
A. Bacterial1. Campylobacter jejuni. Most commonly from a foodborne exposure to
poultry.
2. Salmonella spp
a. Nontyphoid. Most commonly from a foodborne exposure to poultry or eggs.
b. Typhoid and paratyphoid. Person-to-person contact during international travel.
3. Shigella spp. Person-to-person contact.
4. Shiga toxin–E coli (0157:H7). Most commonly a foodborne exposure to undercooked beef or raw seed sprouts.
5. Vibrio spp
a. Cholera. Low level of endemicity in U.S. Gulf Coast states with transmission by water exposure or seafood exposure.
b. Noncholera. Most commonly foodborne exposure to shellfish and seafood.
6. Yersinia enterocolitica. Can be associated with swine and cattle exposure.
7. Aeromonas spp. International travel to tropical regions.
8. Plesiomonas shigelloides. International travel and ingestion of seafood.
9. Staphylococcus aureus. Foodborne exposure (eg, potato salad) due to preformed toxin.
10. Clostridium perfringens. Contaminated meat, vegetables, or poultry
with bacterial spores.
11. Bacillus cereus. Contaminated rice (reheated rice) and vegetable sprouts with bacterial spores.
12. Clostridium difficile.
B. Viruses. Most commonly occur during the winter months and are typically due to outbreaks in families, nursing homes, or day care centers (usually selflimiting
and less than one day).
1. Noroviruses.
2. Rotavirus.
3. Enteric adenoviruses (types 40 and 41).
4. Cytomegalovirus (CMV). More common in immunocompromised patients.
C. Parasites. Most commonly related to international travel and/or contaminated
water. Diarrhea usually persists for greater than 7 to 10 days.
1. Giardia intestinalis
2. Cryptosporidium parvum
3. Cyclospora cayetanensis
4. Microsporidia spp
5. Entameba histolytica. (Africa, Asia, Latin America).
6. Balantidium coli. (Asia).
Clinical Manifes tations of Infectious Diarrhea(SYMPTOMS).
A. D iarrhea. Usually one of two forms, but there can be considerable overlap.
1. Watery diarrhea without blood. Usually self-limiting and clinically nonspecific to etiology.
2. Diarrhea with blood (dysentery). Usually indicates colitis (ie, inflammatory diarrhea). Associated with fever, nausea, and abdominal pain and cramps. Most commonly due to Shigella, Campylobacter, nontyphoid Salmonella, and Shiga toxin–E coli. Also, can be associated with Aeromonas spp, Yersinia spp, noncholeraic Vibrio, and E histolytica.
B. Abdominal Pain and Cramps. Usually associated with dysentery but can also occur without dysentery.
C. N ausea and Vomiting. May be associated with abdominal pain and cramps but is typically due to viral illnesses.
D. F ever. Usually occurs with acute dysentery (ie, inflammatory diarrhea) or bacteremia from salmonella.
E. T enesmus. May indicate inflammatory diarrhea and is characterized as a feeling of a constant need to defecate.
F. D elirium or Altered Mental Status. Usually indicates dehydration and is usually associated with other findings such as tachycardia, dry mucous membranes,and poor skin turgor.
Approach to the Patient.A. H istory. A complete history should be performed with attention to exposures or risk factors associated with infectious diarrhea, comorbid illnesses
(immunocompromised or pregnant patients may be at risk for certain infections), medications, recent travel history, and occupation (eg, day care or nursing home worker). Additionally, diarrhea in family members and the timing of diarrhea onset may be helpful:
1. Incubation period less than 6 hours. (S aureus or B cereus.)
2. Incubation period 6 to 24 hours. (C perfringens or B cereus.)
3. Incubation period 16 to 72 hours. (All other causes.)
B. Physical Examination. A complete physical examination should be performed
with focused attention on:
1. Neurologic examination (to assess mental status by the Glasgow coma cale).
2. HEENT examination (dry mucous membranes can suggest dehydration).
3. Cardiovascular examination (resting tachycardia or orthostatic hypotension may suggest dehydration).
4. Musculoskeletal examination (joint pain may suggest Yersinia spp or
C jejuni as Reiter syndrome).
5. Rectal examination (to detect blood in the stool that may indicate dysentery).
Because the most feared complication of infectious diarrhea is dehydration, the clinical evaluation of the degree of dehydration remains important. (The followingare general considerations that would vary among different patients.)
1. Mild-to-Moderate Dehydration (3% to 9% Fluid Loss)
a. Fatigue and restlessness
b. Dry mucous membranes and thirst sensation
c. Weak pulses and cool extremities
d. Decreased urine output (may be indicated by a dark-concentrated urine and with less than 800 mL per day)
2. Severe Dehydration (Greater than 10% Fluid Loss)
a. Apathy and lethargy
b. Dry mucous membranes, sunken eyes, and extreme thirst sensation
c. Deep breaths and tachycardia
d. Skin tenting, poor capillary refill, weak pulses, and cool extremities
e. Minimal urine output (less than 500 mL dark-concentrated urine per day)
C. Laboratory Studies
1. CBC(COMPLETE BLOOD COUNT). Nonspecific. An elevated hematocrit may suggest dehydration.
2. BMP. Infectious diarrhea may produce a non–gap metabolic acidosis in association with electrolyte abnormalities (eg, hypernatremia, hypokalemia). An elevated BUN, creatinine, and metabolic alkalosis may suggest dehydration.
3. Blood cultures. Usually not ordered and of low yield; however, bacteremia may occur with Salmonella spp–related infections.
4. Stool leukocytes and/or lactoferrin. May be helpful for inflammatory diarrhea, but nonspecific.
a. Stool leukocytes. Sensitivity 73% and specificity 84% for bacterial infectious diarrhea. A small content of stool mucus or liquid stool is stained with methylene blue stain or Wright stain and then examined for leukocytes. A false-negative test may occur with cytotoxogenic
C difficile or E histolytica infection due to destruction of leukocytes.
b. Stool lactoferrin. Sensitivity 92% and specificity 79% for bacterial infectious diarrhea. Lactoferrin is a glycoprotein found in neutrophil granules and is detected by a rapid immunologic latex agglutination method. The test performance is not altered by the destruction of
leukocytes.
5. Stool cultures. The diagnostic yield is estimated from 1% to 5%. Indicated when patients have any of the following:
a. Severe diarrhea (greater than 6 stools per day)
b. Dysentery
c. Diarrhea associated with fever
d. Persistent diarrhea (over more than 7 days)
e. Multiple cases of diarrhea
TREATMENT
A. Supportive Care. Should be provided in all cases and can consist of fluid and electrolyte replacement, a diet of easily digestible foods (eg, BRAT diet: bananas, rice, applesauce, and toast), and/or antimotility medications (eg, loperamide). Antimotility medications should be avoided in patients with dysentery or suspected inflammatory diarrhea. Patients should avoid milk or other dairy products due to the development of transient lactose intolerance.
B. Oral Rehydration Therapy. The initial treatment of infectious diarrhea should focus on the prevention of dehydration with rehydration efforts. Commercialformulations (eg, Pedialyte) can be obtained and used according to the listed directions; however, as a general rule, a homemade oral rehydration solution can be produced by the following formula: add 1 tablespoon of salt and
2 tablespoons of sugar to 1 liter of water.Treatment recommendations according to the degree of dehydration include the following. (These are general rules to the approach to rehydration
and may not apply to all patients.)
1. Minimal Dehydration (Less than 3% Fluid Loss)
a. Less than 10 kg weight: 60–120 mL of oral rehydration solution per diarrhea stool
b. Greater than 10 kg weight: 120–240 mL of oral rehydration solution per diarrhea stool
2. Mild-to-Moderate Dehydration (3% to 9% Fluid Loss)
a. May be treated as an outpatient
b. 50–100 mL per kg of body weight replaced over a 3- to 4-hour period of time
B. Epidemiology
1. Infectious diarrhea is the most common cause of diarrhea worldwide.
2. The second most common cause of death worldwide but the leading cause of childhood death worldwide.
3. In the United States, most episodes occur during the winter months and are due to viral pathogens (eg, noroviruses, rotaviruses).
C. D iarrhea Syndromes
1. Acute infectious diarrhea. Lasting less than 14 days.
a. Acute watery diarrhea without blood
b. Acute dysentery (diarrhea with blood)
2. Chronic or persistent diarrhea. Lasting more than 14 days.
D. Pathogenesis. Pathogens are transmitted through contaminated water or foods/food products and reach the gastrointestinal tract to cause:
1. Increased intestinal secretion of fluid and electrolytes, most commonly in the small intestine, through the production of enterotoxins (eg,cholera toxin, Escherichia coli heat labile and heat stable toxins) that may mediate secretagogues (eg, 5-hydroxytryptamine [5-HT]).
2. Decreased intestinal absorption of fluid and electrolytes in the small and large intestine through intestinal mucosal damage. Severe villous atrophy can occur with infection due to Giardia, Cryptosporidium, Cyclospora, and Microsporidium (intestinal protozoa). An alternative cause of villous atrophy is celiac disease (an autoimmune disorder due to gluten intolerance).
CAUSES OF INFECTIOUS DIARRHEA.
A. Bacterial1. Campylobacter jejuni. Most commonly from a foodborne exposure to
poultry.
2. Salmonella spp
a. Nontyphoid. Most commonly from a foodborne exposure to poultry or eggs.
b. Typhoid and paratyphoid. Person-to-person contact during international travel.
3. Shigella spp. Person-to-person contact.
4. Shiga toxin–E coli (0157:H7). Most commonly a foodborne exposure to undercooked beef or raw seed sprouts.
5. Vibrio spp
a. Cholera. Low level of endemicity in U.S. Gulf Coast states with transmission by water exposure or seafood exposure.
b. Noncholera. Most commonly foodborne exposure to shellfish and seafood.
6. Yersinia enterocolitica. Can be associated with swine and cattle exposure.
7. Aeromonas spp. International travel to tropical regions.
8. Plesiomonas shigelloides. International travel and ingestion of seafood.
9. Staphylococcus aureus. Foodborne exposure (eg, potato salad) due to preformed toxin.
10. Clostridium perfringens. Contaminated meat, vegetables, or poultry
with bacterial spores.
11. Bacillus cereus. Contaminated rice (reheated rice) and vegetable sprouts with bacterial spores.
12. Clostridium difficile.
B. Viruses. Most commonly occur during the winter months and are typically due to outbreaks in families, nursing homes, or day care centers (usually selflimiting
and less than one day).
1. Noroviruses.
2. Rotavirus.
3. Enteric adenoviruses (types 40 and 41).
4. Cytomegalovirus (CMV). More common in immunocompromised patients.
C. Parasites. Most commonly related to international travel and/or contaminated
water. Diarrhea usually persists for greater than 7 to 10 days.
1. Giardia intestinalis
2. Cryptosporidium parvum
3. Cyclospora cayetanensis
4. Microsporidia spp
5. Entameba histolytica. (Africa, Asia, Latin America).
6. Balantidium coli. (Asia).
Clinical Manifes tations of Infectious Diarrhea(SYMPTOMS).
A. D iarrhea. Usually one of two forms, but there can be considerable overlap.
1. Watery diarrhea without blood. Usually self-limiting and clinically nonspecific to etiology.
2. Diarrhea with blood (dysentery). Usually indicates colitis (ie, inflammatory diarrhea). Associated with fever, nausea, and abdominal pain and cramps. Most commonly due to Shigella, Campylobacter, nontyphoid Salmonella, and Shiga toxin–E coli. Also, can be associated with Aeromonas spp, Yersinia spp, noncholeraic Vibrio, and E histolytica.
B. Abdominal Pain and Cramps. Usually associated with dysentery but can also occur without dysentery.
C. N ausea and Vomiting. May be associated with abdominal pain and cramps but is typically due to viral illnesses.
D. F ever. Usually occurs with acute dysentery (ie, inflammatory diarrhea) or bacteremia from salmonella.
E. T enesmus. May indicate inflammatory diarrhea and is characterized as a feeling of a constant need to defecate.
F. D elirium or Altered Mental Status. Usually indicates dehydration and is usually associated with other findings such as tachycardia, dry mucous membranes,and poor skin turgor.
Approach to the Patient.A. H istory. A complete history should be performed with attention to exposures or risk factors associated with infectious diarrhea, comorbid illnesses
(immunocompromised or pregnant patients may be at risk for certain infections), medications, recent travel history, and occupation (eg, day care or nursing home worker). Additionally, diarrhea in family members and the timing of diarrhea onset may be helpful:
1. Incubation period less than 6 hours. (S aureus or B cereus.)
2. Incubation period 6 to 24 hours. (C perfringens or B cereus.)
3. Incubation period 16 to 72 hours. (All other causes.)
B. Physical Examination. A complete physical examination should be performed
with focused attention on:
1. Neurologic examination (to assess mental status by the Glasgow coma cale).
2. HEENT examination (dry mucous membranes can suggest dehydration).
3. Cardiovascular examination (resting tachycardia or orthostatic hypotension may suggest dehydration).
4. Musculoskeletal examination (joint pain may suggest Yersinia spp or
C jejuni as Reiter syndrome).
5. Rectal examination (to detect blood in the stool that may indicate dysentery).
Because the most feared complication of infectious diarrhea is dehydration, the clinical evaluation of the degree of dehydration remains important. (The followingare general considerations that would vary among different patients.)
1. Mild-to-Moderate Dehydration (3% to 9% Fluid Loss)
a. Fatigue and restlessness
b. Dry mucous membranes and thirst sensation
c. Weak pulses and cool extremities
d. Decreased urine output (may be indicated by a dark-concentrated urine and with less than 800 mL per day)
2. Severe Dehydration (Greater than 10% Fluid Loss)
a. Apathy and lethargy
b. Dry mucous membranes, sunken eyes, and extreme thirst sensation
c. Deep breaths and tachycardia
d. Skin tenting, poor capillary refill, weak pulses, and cool extremities
e. Minimal urine output (less than 500 mL dark-concentrated urine per day)
C. Laboratory Studies
1. CBC(COMPLETE BLOOD COUNT). Nonspecific. An elevated hematocrit may suggest dehydration.
2. BMP. Infectious diarrhea may produce a non–gap metabolic acidosis in association with electrolyte abnormalities (eg, hypernatremia, hypokalemia). An elevated BUN, creatinine, and metabolic alkalosis may suggest dehydration.
3. Blood cultures. Usually not ordered and of low yield; however, bacteremia may occur with Salmonella spp–related infections.
4. Stool leukocytes and/or lactoferrin. May be helpful for inflammatory diarrhea, but nonspecific.
a. Stool leukocytes. Sensitivity 73% and specificity 84% for bacterial infectious diarrhea. A small content of stool mucus or liquid stool is stained with methylene blue stain or Wright stain and then examined for leukocytes. A false-negative test may occur with cytotoxogenic
C difficile or E histolytica infection due to destruction of leukocytes.
b. Stool lactoferrin. Sensitivity 92% and specificity 79% for bacterial infectious diarrhea. Lactoferrin is a glycoprotein found in neutrophil granules and is detected by a rapid immunologic latex agglutination method. The test performance is not altered by the destruction of
leukocytes.
5. Stool cultures. The diagnostic yield is estimated from 1% to 5%. Indicated when patients have any of the following:
a. Severe diarrhea (greater than 6 stools per day)
b. Dysentery
c. Diarrhea associated with fever
d. Persistent diarrhea (over more than 7 days)
e. Multiple cases of diarrhea
TREATMENT
A. Supportive Care. Should be provided in all cases and can consist of fluid and electrolyte replacement, a diet of easily digestible foods (eg, BRAT diet: bananas, rice, applesauce, and toast), and/or antimotility medications (eg, loperamide). Antimotility medications should be avoided in patients with dysentery or suspected inflammatory diarrhea. Patients should avoid milk or other dairy products due to the development of transient lactose intolerance.
B. Oral Rehydration Therapy. The initial treatment of infectious diarrhea should focus on the prevention of dehydration with rehydration efforts. Commercialformulations (eg, Pedialyte) can be obtained and used according to the listed directions; however, as a general rule, a homemade oral rehydration solution can be produced by the following formula: add 1 tablespoon of salt and
2 tablespoons of sugar to 1 liter of water.Treatment recommendations according to the degree of dehydration include the following. (These are general rules to the approach to rehydration
and may not apply to all patients.)
1. Minimal Dehydration (Less than 3% Fluid Loss)
a. Less than 10 kg weight: 60–120 mL of oral rehydration solution per diarrhea stool
b. Greater than 10 kg weight: 120–240 mL of oral rehydration solution per diarrhea stool
2. Mild-to-Moderate Dehydration (3% to 9% Fluid Loss)
a. May be treated as an outpatient
b. 50–100 mL per kg of body weight replaced over a 3- to 4-hour period of time
