Electrical injury-electric shock

 Electrical injury

Electrical injury is the damage caused by an electrical current passing through the body. An electrical injury can be mild or severe, its severity depending on Kouwenhoven’s factors:

●Type of current, direct (DC), or alternating (AC). AC is substantially more dangerous than DC. AC may cause tetanic muscle contraction, making the victim unable to release the electrical source. This may lead to an increased duration of current delivery. In contrast, DC usually causes a single intense muscle contraction, which often thrusts the victim away from the electrical source, resulting in a smaller duration of current flow through the body.

●Voltage: High voltage (>600 V)  is generally associated with greater morbidity and mortality, although fatal injury can occasionally occur at household current ( which may induce ventricular fibrillation). High-voltage injuries may cause massive internal burns and coagulation necrosis of soft tissues (such as muscle), along with edema, which may lead to compartment syndrome.

●Duration of exposure (longer exposure is associated with more severe damage)

●Body resistance

●Pathway of current (which determines the specific tissues damaged)

Manifestations of electrical injury range from skin burns to damage to internal organs, cardiac arrhythmias, and respiratory arrest. Electrical injuries are classified into those of low voltage (≤1000 V) and high voltage (>1000 V).

Pathophysiology

The mechanisms of electricity-induced injury are the following:
►Electric current causes damage to cell membranes leading to electrolyte abnormalities and cellular edema. This is eventually followed by irreversible cell damage and cell death. This process is called electroporation. Electrical injury also alters cell membrane resting potential leading to muscle tetany.
►Another mechanism of tissue damage is thermal injury to the tissues, occurring when electrical energy is converted to thermal energy causing coagulative necrosis of the tissues.
►Τhe flow of current through the tissue can cause thermal injury to the vascular endothelium and associated thrombosis.
►Mechanical injury (trauma) due to falls or violent muscle contraction.

Clinical presentation of the patient with an electric injury

The following tissues and organs can be affected by an electrical injury, depending on the severity of the incident:

The skin:
Electrical injury is often associated with partial- or full-thickness burns at entrance and exit sites. Another type of burns associated with electrical injury are arc burns, or “kissing burns” occurring when electricity jumps from a skin surface to another skin surface that is in direct contact with the first. This typically occurs across flexed areas of the body.
In some cases, clothing may catch fire resulting in thermal burns.
Important note: The size of the skin injury does not correlate well with the severity of internal injuries which can often be more extensive in cases of electrical injury.

The cardiovascular system:

An electrical injury can cause arrhythmias. The most severe arrhythmias (ventricular fibrillation ventricular tachycardia, asystole) may occur immediately and they may result in immediate cardiac arrest. In patients presenting in cardiac or respiratory arrest immediate resuscitation is needed (cardiopulmonary resuscitation) according to the ACLS protocols. Other arrhythmias such as sinus tachycardia or bradycardia, atrial fibrillation, and atrial or ventricular ectopic beats may appear immediately or in a delayed fashion following electrical injury.
Electrical injury can cause transient ECG abnormalities such as ST-segment elevations (resembling an acute myocardial infarction), or T wave flattening or inversion without true myocardial ischemia being present. Another ECG abnormality that may appear is a prolonged QT interval. Less commonly, direct injury to the myocardium with a decreased ejection fraction (EF) depicted by echocardiography, or injury to the coronary arteries causing a myocardial infarction may occur.
Vascular injury is most prominent at the intimal and medial layers of the vascular wall and it may lead to thrombosis causing tissue ischemia or aneurysmal dilation and hemorrhage (later). Decreases in tissue perfusion lead to edema and tissue death. Areas of infarction may be distributed sporadically throughout the injured region, with areas of surviving tissue adjacent to necrotic tissue.

A serious high-voltage electrical injury, because of the extensive soft tissue destruction (like an extensive burn injury), can cause massive fluid shifts, i.e. loss of fluid from the intravascular space. Thus, it is important to monitor the patient's hemodynamic status and urine output (via a Foley catheter) and adequate intravenous fluid replacement will be required.   

Respiratory system:
Respiratory arrest may occur either as a result of tetanic paralysis of the respiratory muscles or of damage to the brainstem respiratory center. Apnea due to respiratory arrest may result in hypoxic cardiac arrest. Other complications from the respiratory system may include pulmonary edema, pulmonary contusion (as a result of trauma) and aspiration pneumonia.

Nervous system
Electrical injury may often involve the central and peripheral nervous systems. The most common immediate symptoms from the central nervous system (CNS) are confusion, transient loss of consciousness, agitation, coma or seizures. Seizures are common. They may appear as a transient isolated event or as a lasting seizure disorder. Immediately after electrical injury transient spastic paralysis with accompanying sensory deficits may occur. Cerebral infarction may result from arterial injury. Traumatic injury (which is common in patients with electrical injury) may cause complications, such as intracranial hemorrhage.
Late sequelae may follow, such as spinal cord dysfunction, peripheral neuropathy, cognitive impairment, insomnia and emotional lability.

Musculoskeletal system
At the time of admission of the patient with electrical injury complete neurovascular exam of each extremity should be done and documented.
Muscle necrosis may occur primarily due to electrical injury, or it may develop secondary to an impairment of blood supply. Tissue edema may result in the development of compartment syndrome, which requires fasciotomy. 

Compartment syndrome is a common limb-threatening risk of electrical injury. The typical signs and symptoms of compartment syndrome (5 Ps: Pain Pallor, Paresthesia, Pulselessness, Paralysis) are less reliable in the setting of electrical injury. Diagnostic difficulties may arise because patients may have pain from cutaneous burns or paresthesias from nerve injury. Careful clinical evaluation is required for the diagnosis of compartment syndrome: tightness of the involved area to palpation, pain with flexion or extension, or fixed flexion. Diagnosis should be made before the development of pulselessness and paralysis, which are late signs of compartment syndrome.
Another risk of severe electrical injury is rhabdomyolysis which may cause acute renal failure. The diagnosis of rhabdomyolysis is based on the presence of elevated creatine phosphokinase (CK or CPK), myoglobinuria, and/or elevated serum potassium.

Trauma
An electrical shock can cause injury due to powerful muscle contractions or falls (eg, from a ladder). This may result in dislocations (e.g. shoulder dislocation), fractures (e.g. vertebral or long bone fractures) and blunt injuries to internal organs.

Head
Young children who bite electrical cords develop partial or full-thickness burns in their mouth and lips. Labial artery hemorrhage may occur 5 to 10 days after the electrical injury in some of these children, when the eschar separates. Such burns may also result in several late sequelae, such as cosmetic deformities and impaired growth of the teeth.
Ocular involvement is not uncommon after an electrical injury, especially cataracts and less commonly corneal or conjunctival burns, or retinal detachment.
Regarding the auditory system, vertigo commonly occurs, which may be transient or persistent, whereas the development of sensorineural deafness is rare.

 

Treatment of patients with electrical injury

Always turn off the power source before approaching the victim. Particularly for high-voltage injuries, involvement of authorized personnel, such as the local power company, in disconnecting the power source may be required.
After disconnecting the power source, assess the cardiopulmonary status of the patient (ABC: airway-breathing-circulation), obtain an ECG, begin cardiac monitoring, check oxygen saturation with a pulse oximeter and establish intravenous access. When head or neck trauma is possible, ensure cervical spine immobilization. Inline immobilization of the spine is one of the top priorities in a patient with trauma.
In patients with extensive burns of the face, mouth, or neck, endotracheal intubation should be provided early, as soft-tissue swelling can develop rapidly and compromise the airway.
Low-voltage electrical injuries (< 240 V) with minimal symptoms, normal physical exam, and normal ECG generally require only local wound treatment and they are not admitted to the hospital.
Patients presenting in cardiac arrest should be treated immediately according to the ACLS protocols.
Cardiac monitoring for 24 hours after the electrical injury is indicated in patients with:
● high-voltage injury
● abnormal ECG or presence of arrhythmias
● initial loss of consciousness
● chest pain
Patients without any of the above presenting features do not require cardiac monitoring.
Pain is controlled with opioid analgesics. NSAIDs should be avoided in these patients because of the risk of acute kidney injury (which may result from myoglobinuria, or from hypoperfusion of the kidneys in cases with hypotension and large intravascular volume losses).
Patients with a severe electrical injury involving possible extensive deep tissue damage will need intravenous (IV) fluid administration.
During the primary survey of the patient, IV crystalloid solution (lactated Ringer’s) should be started for adults at a rate of 500ml/hr, for children of age between 6-13 years at 250ml/hr and for children < 6 years should be started at 125ml/hr.
During the secondary survey burn size should be assessed and the starting IV fluid rate should be calculated according to the formula:
4ml x Body Weight (in kg) x %TBSA / 16 , 

where % TBSA= the estimated percentage of the total body surface area with second or third-degree burns. This initial fluid administration rate should then be adjusted on the basis of urine output, in order to achieve a urine output goal of 30ml/hr if myoglobinuria is not present. In the presence of myoglobinuria, urine output goal is 75-100 ml/hr, until myoglobinuria clears.
Injured extremities require burn wound management and they should be monitored for the possible development of compartment syndrome. In patients with an electrical injury, the visible burn wound often hides a more significant and extensive injury that lies beneath, within the deep tissue. Subsequent edema may develop leading to vascular compromise to any area distal to the injury. Thus, circulation to distal vascular beds should be repeatedly assessed because immediate escharotomy and fasciotomy may be required. The burn injury is treated with early exploration and debridement of devitalized tissues. Tissue with questionable viability is left in place, with planned repeated exploration of the wound in 48 hours. Depending on the severity of the wound, repeated explorations may be required until the wound is completely debrided because electrical damage to vessels may be delayed. Therefore, the extent of necrotic tissue may increase after the initial debridements. After the devitalized tissues are removed, closure of the wound is performed by an experienced surgeon with skin grafts or flaps.

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 Bibliography

Walls RM, Hockberger RS, Gausche-Hill M. Rosen’s emergency medicine: concepts and clinical practice. 9th edition. Philadelphia, PA : Elsevier, 2018.

Arnoldo B, Klein M, Gibran NS. Practice guidelines for the management of electrical injuries. J Burn Care Res. 2006;27(4):439-447. LINK https://academic.oup.com/jbcr/article-abstract/27/4/439/4605406?redirectedFrom=fulltext&login=false

 Leibovici D, Shemer J, Shapira SC. Electrical injuries: current concepts. Injury. 1995;26(9):623-627

Gentges J et al. Electrical injuries in the emergency department: An evidence-based review. Emerg Med Pract 2018;20(11):1-20  https://pubmed.ncbi.nlm.nih.gov/30358379/

Lillard P, Markuns K . Guidance for Emergency Medical Management of Electrical Injuries
LINK http://www.masscosh.org/sites/default/files/documents/Guidance%20for%20Emergency%20Medical%20Management%20of%20Electrical%20Injuries.doc

Family Practice Notebook- Electrical injury LINK  https://fpnotebook.com/er/environ/ElctrclInjry.htm

Heat illness : Heat exhaustion and heat stroke 

Exposure to high temperatures and high humidity, as well as strenuous exercise may lead to heat illness, a continuum of disease that encompasses disorders ranging in severity from muscle cramps, heat-syncope and heat exhaustion to heat stroke. Heat stroke is a life-threatening emergency, thus it is the most severe form of heat illness. Heat illness can affect individuals exposed to environmental conditions of high temperature such as athletes, construction workers, firefighters, military personnel, etc, or individuals staying in a hot environment, especially if they have predisposing factors reducing the body’s ability to dissipate heat. 

Such predisposing factors are:

Age extremes (children, elderly)

Obesity

Dehydration (e.g. gastroenteritis, inadequate fluid intake)

Cardiovascular disease, such as congestive heart failure

Certain endocrine and metabolic diseases, such as diabetes mellitus and hyperthyroidism

A febrile infection

Alcohol, cocaine

Treatment with some categories of medications, such as:

MAO inhibitors, antipsychotics, anxiolytics

Anticholinergics

Diuretics

Beta-blockers

 

 Exertional heat illness is one of the leading causes of death among young athletes and may be on the rise because of the increasing popularity of mass-participation athletic events. Early recognition and treatment of EHI is very important because it can reduce associated morbidity and mortality.

Pathophysiology of heat illness

 Heat is generated by the basal metabolism, by muscular activity and it is also absorbed from a warm environment.

The human organism has homeostatic mechanisms to maintain normal core body temperature. An increase in core temperature is detected in the hypothalamus, which reacts by sending signals to induce cutaneous vasodilation and sweating.

Under normal conditions, the body is able to dissipate heat through:

■Radiation: Transfer of heat directly from the body to a cooler environment by infrared radiation. This mechanism does not require air motion or direct contact

■Evaporation: Cooling of the skin by water vaporization (eg, sweat)

■Convection: Transfer of heat to cooler air (or liquid) that passes over exposed skin

■Conduction: Transfer of heat from the skin to a cooler surface that is in direct contact to the skin.

The contribution of each of these mechanisms depends on environmental temperature and humidity. When the environmental temperature is not high, radiation has a major role (65%), evaporation of sweat is also important (normally provides 30% of cooling). Exhalation of water vapor and production of urine and feces provide about 5% of cooling. When the environmental temperature is > 35° C, evaporation accounts for virtually all dissipation of heat because the other mechanisms can function only when the environmental temperature is significantly lower than body temperature. Radiation, convection, and conduction are decreasingly effective as the temperature of the environment approaches the skin’s temperature. Therefore, in such conditions of a hot environment, only evaporation is effective. However, evaporation is influenced by humidity and it is ineffective above a relative humidity of 75%.

 Despite the compensative mechanisms of the body significant or prolonged exposure to heat may exceed the capacity of these physiologic cooling mechanisms. This will lead to an elevated core temperature. The body can tolerate modest, transient core temperature elevations, but severe elevations (> 41° C) are not well tolerated. Severe core temperature elevations can result in protein denaturation and the release of inflammatory cytokines. This causes cellular dysfunction and dysfunction of multiple organs. The activation of the inflammatory cascade apart from causing organ dysfunction may also lead to the activation of the coagulation cascade resulting in the development of disseminated intravascular coagulation (DIC). The pathophysiologic process is similar to the pathophysiology of multiple organ dysfunction syndrome, which occurs in patients with prolonged circulatory shock.

 

Mild forms of heat illness

Heat edema manifests by mild swelling of the feet, ankles, and hands that appears within the first few days of exposure to a hot environment. It is caused by cutaneous vasodilatation and orthostatic pooling of interstitial fluid in gravity-dependent extremities when a person is sitting or standing for a long time in a hot environment. The body’s response to a hot environment may often cause an increase in the secretion of aldosterone and antidiuretic hormone which also contributes to edema formation.  Generally, edema is the clinical manifestation of an accumulation of fluid within the interstitial spaces. It develops when the normal balance between the flow of fluid out of capillaries and the return of fluid into the vascular space via capillary reabsorption and lymphatic flow is disrupted. Heat edema is mild and self-limited, usually resolving spontaneously in a few days. Elevation of the legs is usually helpful to reduce swelling. Diuretics are not used for heat edema (They are used for edema due to other causes, such as congestive heart failure or hepatic failure).

Heat stress or heat exhaustion

Heat exhaustion is a form of heat illness of moderate severity that occurs when the body overheats exceeding the capacity of it’s cooling homeostatic mechanisms, as a result of physical activity in a hot environment. The principal underlying pathophysiologic mechanism of heat stress is water and sodium depletion. Typically there is a combination of both. Water depletion is the predominant feature in the elderly and in people working in a hot environment with inadequate water replacement. Salt depletion predominates in individuals who replace fluid losses with large amounts of water or hypotonic solutions.

Manifestations of heat exhaustion may include thirst, cramps, dizziness, headache, vertigo, anorexia, nausea and vomiting but there are no severe manifestations from the central nervous system (this differentiates it from heat stroke). The patient is flushed and sweating (with sweaty hot skin). The rectal temperature is usually 38-39°C  (< 40°C).  Τachycardia and orthostatic hypotension occur as a result of dehydration. Heat stress (heat exhaustion), if not adequately treated, may progress to heat stroke, which a is a severe condition (see below).

Treatment of heat exhaustion

The patient must rest in a cool environment in supine position with leg elevation. Volume and electrolyte replacement is required either with oral electrolyte solutions in patients with mild heat stress, or with IV fluids (1 - 2 L of normal saline) in patients suffering from a more severe form of heat exhaustion with vomiting or with manifestations of significant tissue hypoperfusion. Active skin cooling by sponging or spraying with water and using a fan is usually necessary.

 

Heat stroke

Heat stroke is a medical emergency characterized by extremely elevated core body temperature > 40,5 °C (usually ≥ 41 °C) and central nervous system dysfunction manifested by confusion, delirium, seizures or coma, that occurs after exposure to a very hot environment and/or strenuous physical activity. It is often accompanied by hepatic damage and rhabdomyolysis. If it is not treated promptly, it may lead to multiorgan dysfunction because the extremely elevated body temperature can cause damage to the tissues.

There are two categories of heat stroke

Classic heat stroke is caused by passive exposure to a hot environment resulting in an imbalance between heat production by and dissipation from the body. More susceptible for heat stroke are young children, pregnant women, the elderly and individuals with chronic underlying disease.

Exertional heat stroke is caused by high intensity physical activity leading to an imbalance between heat production by and dissipation from the body. It is common among healthy people who engage in intense activity during the summer, such as athletes, soldiers, firefighters and construction workers.

Manifestations and diagnosis of heat stroke

The diagnosis of heat stroke requires not only the presence of an extremely elevated core temperature of the body but also the presence of severe manifestations from the central nervous system (see below) and conditions of exposure to a hot environment and/or intense physical activity in a hot environment.

Manifestations of heat stroke:

Elevated core body temperature > 40,5 °C (105°F)

Hot skin (due to vasodilation). The skin is often (but not always) dry. Sweating may occasionally be present if the patient is not significantly dehydrated.

Manifestations of severe central nervous system dysfunction (confusion, hallucinations, delirium, seizures or coma)

Tachycardia, wide pulse pressure. Hypotension may be present. These cardiovascular manifestations are due to peripheral vasodilation

Tachypnea

Rales may be present due to noncardiogenic pulmonary edema (acute respiratory distress syndrome-ARDS)

Hypoxemia may be present as a result of noncardiogenic pulmonary edema or aspiration

Complications of heat stroke may include rhabdomyolysis, acute renal failure (caused by rhabdomyolysis, severe dehydration, or direct thermal injury to the kidneys ) , shock, acute respiratory distress syndrome (ARDS), reversible liver damage,  disseminated intravascular coagulation ( DIC), and multiple organ failure.

Treatment of heat stroke

 Priorities are the ABCs (assess and treat airway, breathing and circulation) and rapid initiation of cooling if the rectal temperature is ≥ 40  °C with a target to achieve rectal temperature of 38,5 to 39 °C .  Remove clothes, spray or sponge the skin with tepid water and use a fan to encourage evaporation. Ice packs on the neck, axilla and groin are also used.  Another method of cooling is immersion cooling, by placing the patient in a tub with cold water so that the torso and extremities are covered with water. In refractory cases, cold gastric or peritoneal lavage and cold intravenous fluids (cool N/S at 5-10 °C) can be used. Stop cooling therapy at 39°C (102°F) to avoid overshooting and hypothermia. In heat exhaustion or heat stroke antipyretic agents are not helpful because the elevated body temperature is not due to a change in the set point in the hypothalamus. In some cases, during cooling seizures may occur and can be treated successfully with benzodiazepines. 

In patients with heat stroke or heat exhaustion rehydration is needed to replace fluid losses. Initial rehydration is accomplished with prompt administration of  0.5-1.0 L 0.9% normal saline (N/S). Aggressive fluid resuscitation is required until BP >90/60 or central venous pressure (CVP) >12 mL H₂O. Avoid overhydration, which can contribute to pulmonary edema and ARDS. IV fluids should be administered at a rate that ensures adequate urinary output. Hypotension is a common initial finding in heat stroke and it usually responds to treatment with IV crystalloids (N/S).  If hypotension is refractory to IV fluids,  administer vasoactive catecholamines such as dopamine or dobutamine.

Endotracheal intubation and mechanical ventilation is indicated in patients with significantly altered mental status or severe hypoxia.

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LINK: Emergency medicine book-Table of contents

Bibliography

Liu SY, Song, JC, et al. (2020). Expert consensus on the diagnosis and treatment of heat stroke in China. Military Medical Research 2020; 7(1). https://doi.org/10.1186/s40779-019-0229-2

Leiva DF, Church B. Heat Illness. [Updated 2021 Apr 15]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2021 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK553117/

Glazer JL. Management of heatstroke and heat exhaustion. Am Fam Physician. 2005;71(11):2133-2140. PMID: 15952443. LINK https://www.aafp.org/afp/2005/0601/p2133.html

Wilderness Medical Society Practice Guidelines for the Prevention and Treatment of Heat Illness: 2019 Update. LINK https://survive-student-resource.austererisk.com/environmental/wms_heat_illness.html

Bart A English W Diagnosis and management of heat stroke. LINK https://anaesthesiology.gr/media/File/pdf/WFSA_tutorial_341.pdf

 

Cardiac arrest, cardiopulmonary resuscitation (CPR) and advanced cardiac life support (ACLS)

Cardiac arrest is the cessation of effective circulation and is characterized by:

►Unresponsiveness (the patient is unconscious and totally unresponsive)
►Pulselessness (there is no palpable carotid or femoral pulse)
►Little to no respiratory effort (the patient usually is not breathing at all, or has only ineffective agonal respirations, i.e. slow, irregular, shallow gasping respirations that may persist for a few minutes).

Note: Agonal breathing involves slow, irregular short gasps of air (“shallow half-breaths” which often sound like snoring or gasping) while the patient is unconscious and unresponsive. Agonal breathing occurs in approximately 40% of sudden cardiac arrest cases. It is caused by the lower brainstem getting deprived of oxygen and producing an involuntary breathing reflex as a result of this hypoxic stimulus. It is essential not to mistake agonal breathing for real breathing and respond promptly to cardiac arrest victims in need, by starting immediately basic life support (BLS).
Other emergencies that can cause agonal breathing include ischemic stroke involving the brainstem and hemorrhagic stroke. These situations involve restricting blood flow to the brain and this stimulates an involuntary agonal respiration reflex.

If corrective measures are not taken rapidly (such as cardiopulmonary resuscitation-CPR and defibrillation as early as possible in the presence of a shockable rhythm), sudden cardiac arrest progresses to sudden death.

Recognition of cardiac arrest 

By the lay rescuer: 

If a victim is unconscious and unresponsive,
with absent or abnormal breathing (ie, only gasping), the lay rescuer should assume the victim is in cardiac arrest ask for help (alert the emergency medical service) and begin CPR immediately
By a healthcare professional:  

If a victim is unconscious and unresponsive, with absent or abnormal breathing (ie, only gasping), the healthcare provider should check for a (carotid) pulse for 5-10 seconds (not more than 10 seconds). If no definite pulse is felt, the healthcare provider should assume the victim is in cardiac arrest, ask for help (alert the emergency medical service) and begin CPR immediately.

Epidemiology and prognosis of cardiac arrest

Epidemiology and prognosis: 60% of cardiac arrests occur out of the hospital and the overall mortality is 90% (10% survival rate) In the case of out-of-hospital cardiac arrests witnessed by bystanders capable of performing CPR survival rate is about 20%. In-hospital cardiac arrests have an overall survival rate of about 20-30%. The incidence of sudden cardiac arrest increases with age and it is more common in men (57% of the cases).

The cardiac rhythm on presentation is:
● A shockable rhythm in about 25 % of the cases (a cardiac rhythm that can respond to an electric shock delivered by a defibrillator, such as ventricular fibrillation-VF or ventricular tachycardia –VT). In this situation, the survival rate is > 30%.
● A non-shockable cardiac rhythm in about 75% of the cases, such as asystole or pulseless electrical activity (PEA). In these cases, the prognosis is much worse, with a survival rate of about 10%.

Cardiac rhythm in victims of cardiac arrest

Shockable cardiac rhythms include:

●Ventricular fibrillation (VF). VF is characterized by rapid and irregular ventricular electrical activity which renders the ventricles unable to contract in a synchronized manner, resulting in immediate loss of cardiac output. The ECG monitor shows chaotic irregular deflections of varying amplitude and no identifiable P waves, QRS complexes, or T waves. The amplitude of these fast and completely irregular waves decreases with duration (initial coarse VF with large waves progresses to fine VF with waves of small amplitude and ultimately the rhythm will degenerate into asystole, due to progressive depletion of myocardial energy stores).

                     

Coarse VF

                                                                                                                                         

Fine VF

●Pulseless ventricular tachycardia (pulseless VT)

Pulseless VT is a very rapid tachycardia with wide QRS complexes (> 120 milliseconds) that can be monomorphic (no variation of the QRS from beat to beat) or polymorphic ( QRS changes from beat to beat). The most common cause of pulseless ventricular tachycardia is cardiac ischemia. In pulseless VT the rapid ventricular contractions, result in a markedly decreased ventricular filling, leading to a dramatic decrease in cardiac output. As a result, a pulse is absent.

                                 

monomorphic VT

                                               

                           Polymorphic VT torsade de pointes (French for "twisting of the points", a type of polymorphic Ventricular Tachycardia).

                                                                                           

                                                                            

A non-shockable rhythm is 

either

●Asystole ( absent cardiac electrical activity with a straight line displayed on the monitor)

or

●Pulseless electrical activity (PEA)

PEA ( previous term electromechanical dissociation) is characterized by unresponsiveness and the lack of a palpable carotid pulse in the presence of organized cardiac electrical activity. In PEA the monitor shows an organized cardiac rhythm which may be a supraventricular rhythm (sinus or non-sinus) or a ventricular rhythm (accelerated idioventricular rhythm or a ventricular escape rhythm) but there is no effective cardiac contraction and this results in the absence of effective circulation and thus the absence of a palpable pulse.
                                                

Factors affecting survival:

Initial rhythm
Time from the moment of cardiac arrest to the beginning of cardiopulmonary resuscitation-CPR)
Time to first defibrillation attempt (in the presence of a shockable cardiac rhythm)
Total time that the patient is in the state of cardiac arrest
Age of the victim and underlying cause of cardiac arrest

Causes of cardiac arrest:

●Coronary artery disease (the most common cause) 

Cardiac arrest may occur in acute myocardial ischemia (acute coronary syndrome) or in patients with chronic ischemic cardiomyopathy due to a previous myocardial infarction.

●Cardiomyopathies (hypertrophic cardiomyopathy, arrhythmogenic cardiomyopathy-ARVC, dilated cardiomyopathy)

●Valve disease (especially severe aortic stenosis/ very rarely mitral valve prolapse)

●Electrical conduction abnormalities (disorders of cardiac ion channels such as long QT syndrome, short QT syndrome, Brugada syndrome, catecholaminergic ventricular tachycardia/ Wolff- Parkinson- White syndrome due to the presence of an accessory pathway with the capability of rapid conduction between the atria and the ventricles)

●Cardiac tamponade

Non-cardiac etiologies of cardiac arrest:

●Metabolic disorders (especially severe electrolyte abnormalities)

●Toxic ingestions (ingestion of some toxic substances or drug overdose can induce cardiac arrest)

●Acute pulmonary embolism,

●Tension pneumothorax

●Severe infection (sepsis)

●Trauma with massive hemorrhage and circulatory shock

●Intracranial hemorrhage

●Hypothermia

● Electrocution

●Severe hypoxemia

●Primary respiratory arrest 

(Primary respiratory arrest can be due to a central nervous system disorder, adverse drug effect such as opioid overdose, upper airway obstruction due to a foreign body, unconsciousness, and loss of muscular tone leading to the displacement of the posterior portion of the tongue to occlude the oropharynx, pharyngolaryngeal inflammation in acute anaphylaxis, croup, epiglottitis, laryngeal trauma/ lower airway obstruction due to severe bronchospasm, airspace filling disorders (eg, pneumonia, pulmonary edema, pulmonary hemorrhage, drowning).

Respiratory arrest and cardiac arrest are conditions that without prompt and effective treatment, inevitably one will lead to the other.

Initial treatment (resuscitation) of the patient with cardiac arrest

If a person is unconscious with absent breathing or abnormal breathing, alert the emergency medical services (EMS) immediately. A lone bystander with a mobile phone should dial the EMS number, and use a hands-free option (such as the speaker) on the mobile phone and immediately start cardiopulmonary resuscitation (CPR).

Ensure that the scene is safe before approaching the patient.

Chest compressions should be started as soon as possible with the cardiac arrest victim lying on a firm surface whenever feasible. Chest compressions are delivered on the lower half of the sternum.

The heel of one hand is placed on the center of the patient’s chest ( on the lower half of the sternum) and the heel of the other hand

on top of the first. Thus, the hands are overlapped.

Compression depth should be at least 5 cm (2 inches) but not more than 6 cm and compression rate 100-120/ min, with as few interruptions as possible. Allow the chest to recoil completely after each compression. This will allow for the heart to adequately refill with blood between compressions. If possible, rotate the person providing chest compressions every 2-4 minutes (ideally every 2 minutes) to avoid fatigue. Rescuer fatigue could result in suboptimal depth and rate of the chest compressions delivered.

The technique of chest compressions in basic life support (BLS)

Rescue breaths 
Every 30 chest compressions should be followed by 2 rescue breaths and this sequence (30:2) is continued. Airway patency should be maintained using the head tilt-chin lift or the jaw thrust maneuver and any visible foreign bodies in the oral cavity should be removed. The head tilt-chin lift maneuver is used to maintain an open airway when trauma is not suspected, whereas if trauma is suspected use the jaw thrust maneuver to open the airway, in order to avoid moving the cervical spine. For a description of these maneuvers see chapter Emergency airway management and ventilation procedures.

To deliver rescue breaths use a bag-mask device (connected to an oxygen source if available), or a pocket mask, or mouth to mouth technique. When using a mask (a bag-mask device), an airway adjunct (eg, oropharyngeal and/or nasopharyngeal airway) in unconscious patients with no cough or gag reflex can be useful to maintain upper airway patency. An oral airway is preferred
compared with a nasopharyngeal airway when a basal skull fracture is suspected or in a patient with a significant coagulopathy.

 Each rescue breath should be delivered over 1 second with sufficient tidal volume to result in a visible chest rise. Note that you should provide a rescue breath until there is a visible chest rise avoiding over-ventilation (excessive ventilations), which can be harmful.

When providing CPR without an advanced airway, pause compressions (each time a sequence of 30 compressions has been completed) to deliver 2 breaths, each given over 1 second.

Rescue breaths: Mouth to mask technique

If you are unable to provide ventilations, give only continuous chest compressions. Although ventilation with rescue breaths is important, not everyone is willing to perform mouth-to-mouth breathing due to concerns over infectious disease transmission. Chest compressions alone can be effective and should be performed even if rescue breaths are not being delivered.
If the cardiac arrest victim is not intubated, with a single rescuer or with two rescuers two ventilations (rescue breaths) should be given after every 30 compressions. 

In the case of a patient with an advanced airway in place (laryngeal mask airway-LMA or endotracheal tube) and two rescuers, ventilations should be given at a rate of 8 - 10 /minute, without interrupting chest compressions. (Approximately one breath every 6 seconds). Using quantitative waveform capnography during cardiopulmonary resuscitation in intubated patients is recommended by the  2020 AHA Guidelines for ACLS. The purpose of using waveform capnography is to monitor CPR quality (optimize the effectiveness of chest compressions), and also to detect the return of spontaneous circulation (ROSC) during chest compressions. For more information about capnography see Note 3, below.

If a defibrillator (either an automatic external defibrillator-AED, or a manual defibrillator) is available, use it promptly (after at least 1-2 minutes of CPR) to assess the underlying cardiac rhythm and to provide a shock (defibrillation) if a shockable rhythm (VF or pulseless VT) is identified.

 Turn on the defibrillator, connect the defibrillator pads, and the monitor to the patient and assess the patient’s cardiac rhythm. If there is a shockable rhythm, do not delay defibrillation to provide additional CPR once the defibrillator is ready. The general rule is that defibrillation should be performed as soon as possible in the case of a shockable rhythm. In this case, ensure that nobody touches the patient and give an asynchronous electric shock. The first shock should be of an energy 120-200 J if the defibrillator delivers a biphasic shock, or 360 J in the case of an older generation defibrillator that delivers a monophasic shock). Immediately resume CPR after defibrillation (don’t pause to check the cardiac rhythm).
After 2 minutes of CPR check the rhythm. Defibrillate again, if needed (if a shockable rhythm persists) using a higher energy level. When using a defibrillator, provide five cycles (or 2 min) of CPR between rhythm checks. Interruptions in chest compressions to check for the rhythm and for return of spontaneous breathing and carotic pulse should not last more than 10 seconds. Checking for the pulse should last not less than 5 seconds but also not more than 10 seconds, and at the same time (concomitantly) check for the return of spontaneous breathing.

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Drug administration in cardiac arrest and advanced life support (ALS)

While CPR is continuously performed, another rescuer should establish a route for drug and fluid administration ( a peripheral –usually antecubital- intravenous catheter). If an intravenous (IV) line cannot be placed then the intraosseous (IO) route is used. New evidence suggests that the IO route may be less efficient compared with the IV route. Therefore, providers should first attempt establishing IV access for drug administration in cardiac arrest. The IO route may be considered if attempts at IV access are unsuccessful or not feasible. Drug administration by central venous access (by internal jugular, subclavian or femoral vein) may be considered
by skilled physicians (well trained and experienced in these techniques) when other access routes are not available. Although central venous access may achieve more rapidly, higher drug concentrations than peripheral IV, it takes more time and skill to perform. ( Also see chapter Peripheral and central venous cannulation technique ). Endotracheal drug administration may be used when all other access routes are not available but it is regarded as the least-preferred option because it is associated with lower drug concentrations.

The administration of adrenaline (epinephrine) is important in cardiac arrest because, in 2 randomized clinical trials, epinephrine increased return of spontaneous circulation (ROSC) and survival.
For adult patients in cardiac arrest with a shockable rhythm administer adrenaline (epinephrine) 1 mg IV (or IO) after the third shock. ( 1 amp of 1 mg adrenaline is drawn into a syringe and normal saline is added so that the total volume of the solution is 10 ml -1:10.000 adrenaline solution). Immediately after giving IV adrenaline also administer a 20 ml IV push of normal saline.

During continued advanced life support (ALS) repeat adrenaline 1 mg IV (or IO) every 3-5 minutes. 
Give amiodarone 300 mg IV (or IO) for adult patients in cardiac arrest who are still in ventricular fibrillation (VF) or pulseless ventricular tachycardia (pulseless VT) after three shocks have been administered. Amiodarone should only be used after defibrillation and adrenaline (epinephrine) have failed to convert VT or VF.
A further dose of amiodarone 150 mg IV (or IO) should be administered to adult patients in cardiac arrest who are in VF or pVT after five shocks have been administered.

For adult patients in cardiac arrest with a non-shockable rhythm, adrenaline should be administered as soon as possible 1 mg IV ( or IO) as soon as possible and repeated (1 mg adrenaline IV or IO) every 3-5 minutes. Studies indicate that the administration of adrenaline with concurrent high-quality CPR improves survival, particularly in patients with non-shockable rhythms.

In patients with a non-shockable rhythm besides CPR and adrenaline administration, also identification and treatment of any correctable cause of cardiac arrest is essential. In these cases, cardiac arrest generally results from a major cardiovascular, respiratory, or metabolic derangement. Such causes include hypovolemia, hypothermia, hypoxia, hypokalemia,  hyperkalemia, acidosis, severe hypoglycemia, tension pneumothorax, cardiac tamponade, thrombosis (pulmonary embolism or acute myocardial infarction), toxins, trauma.

For the treatment of cardiac arrest, routine administration of calcium, sodium bicarbonate, or magnesium is not recommended.

Note: 1. 

During CPR, interruptions of chest compressions should be minimal (about 5-10 seconds when checking for the carotid pulse and for return of spontaneous respiration). For the delivery of a defibrillator shock, the pause should also be minimized, at about 5 seconds, and this is achieved by continuing chest compressions while charging the defibrillator, stopping compressions to deliver the shock, and starting again the compressions immediately after.

Note 2. 

Airway management in ACLS

After the initiation of CPR and the ALS sequence, if possible consider the progression from simple airway management (head tilt-chin lift or jaw thrust maneuver often with the placement of an oropharyngeal/ and or nasopharyngeal airway with bag-mask ventilation combined with the administration of oxygen) to more advanced airway management (such as a laryngeal mask airway -LMA or an endotracheal tube). (For techniques of airway management see chapter Emergency airway management and ventilation procedures.)  This can be considered when a rescue team member, trained and experienced with these techniques is present. In an attempt for endotracheal intubation (performed only by a well-trained and experienced rescuer) do not interrupt chest compressions for more than 10 seconds.

Note 3. 

The 2020 AHA Guidelines for ACLS recommend using quantitative waveform capnography in intubated patients during CPR. Waveform capnography along with clinical assessment is the preferred method for confirming and monitoring correct placement of an endotracheal tube. It also aids in the assessment of CPR quality (optimization of chest compressions), and detect ROSC (return of spontaneous circulation) during chest compressions. Capnography is a technique that measures expired carbon dioxide (CO₂) which is a metabolic product transferred to the lungs via blood perfusion. The inhaled and exhaled carbon dioxide is graphically displayed on the monitor as a waveform along with its corresponding numerical measurement. The measurement obtained is end-tidal carbon dioxide (ETCO2 or PetCO2). ETCO2) is the level of carbon dioxide that is released at the end of an exhalation. ETCO2 levels reflect the adequacy with which carbon dioxide (CO2) is carried in the blood back to the lungs and also the adequacy with which it is exhaled by the lungs. For this reason, capnography can directly assess ventilation in the lungs, and it also indirectly measures metabolism and circulation. For example, a decrease in perfusion (cardiac output) will lower the delivery of carbon dioxide to the lungs. This will cause a decrease in the ETCO2 (end-tidal CO2). A decrease in ventilation will cause a reduction in the ability of the lungs to exhale CO2 also resulting in a decrease in the ETCO2. Normal ETCO2 in the adult is 35-45 mmHg.

During CPR in an intubated patient, a low ETCO2 value (< 10 mmHg) is an indication that the quality of chest compressions needs improvement. High-quality chest compressions are achieved when the ETCO2 value during CPR is at least 10-20 mmHg.
When ROSC occurs, this will cause a significant increase in the ETCO2 (35-45 mmHg). This is due to a drastic improvement in blood flow (more CO2 is delivered to the lungs by the circulation).

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Bibliography

Patel K, Hipskind JE. Cardiac Arrest. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2021 Jan
LINK https://www.ncbi.nlm.nih.gov/books/NBK534866/

Merchant RM, Topjian AA, et al. ,Part 1: Executive Summary: 2020 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation. 2020;142:S337–S357
 LINK https://www.ahajournals.org/doi/10.1161/CIR.0000000000000918

Perkins, et al., European Resuscitation Council Guidelines 2021: Executive summary,
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The European Resuscitation Council Guidelines for Resuscitation
LINK https://cprguidelines.eu/

Moll V. Overview of Respiratory Arrest. In MSD Manual Professional version
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Kleinman ME, Brennan EE, Goldberger ZD, et al. Adult Basic Life Support and Cardiopulmonary Resuscitation Quality: 2015 American Heart Association Guidelines Update for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation. 2015;132(18 Suppl 2):S414-35.
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Olasveengen TM, de Caen AR, Mancini ME, et al. 2017 International Consensus on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science With Treatment Recommendations Summary. Resuscitation. 2017;121:201-214.

de Vreede-Swagemakers JJ, Gorgels AP, Dubois-Arbouw WI, et al. Circumstances and causes of out-of-hospital cardiac arrest in sudden death survivors. Heart. 1998 Apr;79(4):356-61.
LINK https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1728666/pdf/v079p00356.pdf

Fever, infectious disease and sepsis

Fever, infectious disease and sepsis

The thermoregulatory center in the anterior hypothalamus balances heat production from metabolic activity in muscle and liver with heat loss from the skin and lungs to maintain a normal body temperature of 36.8° ± 0.4°C (98.2°± 0.7°F), with diurnal variation (lower in the morning, higher in the evening).
Fever is one of the most common signs of disease and accounts for

numerous adult and pediatric visits to the emergency department.  Fever is an elevated body temperature: An oral temperature > 37.8 °C  or a rectal temperature > 38°C .

The difference between fever and hyperthermia: 

The site that controls body temperature, i.e. the thermoregulatory center in the hypothalamus has an inherent set point (target temperature) of about 37°C This setpoint ranges from 36° to 37.8°C, affected by the normal daily circadian rhythm. The temperature is lowest around 4 AM and gradually increases during the day, reaching a peak between 6 and 10 PM.

Fever is present when the body's thermostat in the anterior hypothalamus, responding to a disease (usually an infection) resets the target body temperature at a higher level. Pyrogens are substances that cause an elevation of body temperature. Exogenous pyrogens are microorganisms or substances present in microorganisms (e.g the lipopolysaccharide of gram-negative bacteria) , or antigens. Such exogenous pyrogens induce the release of endogenous pyrogens. Endogenous pyrogens such as interleukin-1 (IL-1), interleukin 6, tumor necrosis factor-alpha (TNFa), etc. are cytokines produced by leucocytes and macrophages. Cytokines induce upward displacement of the set point of the thermoregulatory center, via the synthesis of prostaglandin E2.
Hyperthermia is an elevated body temperature that does not result from a resetting of the temperature setpoint by the anterior hypothalamus. The body attempts to maintain the normal temperature but the homeostatic mechanisms, such as vasodilation or increase in the production of sweat, for various reasons are not sufficient to effectively reduce the temperature of the body.
Extreme temperatures >41°C (106°F) almost always are a feature of hyperthermia and not a true fever.
Fever of unknown origin (FUO) is documented fever (38.3°C=101°F or higher temperature) that persists for 2-3 weeks without a diagnosis of the underlying cause despite reasonable investigation (usual definitions set a requirement of at least three outpatient visits or 3-7 days in inpatient care without a diagnosis of the cause).

Pathophysiology of fever

The site of body temperature regulation is the preoptic area of the anterior hypothalamus. This area continuously regulates the balance between heat production and heat loss.

Heat production is controlled by the following mechanisms:

 ►Regulation of the level of circulating thyroxin, the hormone of the thyroid gland. Thyroxin increases cellular metabolism and this results in increased heat production. 

►Increasing muscle activity (shivering when the environment is cold or the shaking chill occurring with fever) is a fast and effective mechanism of heat production
►Regulation of heat production by the hepatic metabolism

Heat loss is regulated by:

►The regulation of the volume of blood that flows to the skin’s surface through vasoconstriction which decreases heat loss and vasodilation, having the opposite effect.

►The amount of sweat production by the exocrine sweat glands. The vaporization of sweat results in cooling the body.

Etiology (causes) of fever 

Disorders causing fever are broadly categorized as : 

►Infectious disease 

(The most common cause of fever is an infection, with viral and bacterial upper and lower respiratory tract or gastrointestinal infections being the most common, followed by urinary tract infection). The list of all possible infectious causes is very extensive. 

►Neoplastic disease (Hodgkin's lymphoma, leukemia, colon cancer, renal adenocarcinoma, cardiac myxoma)

►Inflammatory non-infectious disease 
Collagen or rheumatic diseases and other inflammatory diseases such as systemic lupus erythematosus, Still's disease, Behcet's disease, Crohn's disease, gout, postcardiotomy syndrome
Vasculitis syndromes such as temporal arteritis, polyarteritis nodosa, polymyalgia rheumatica.
Granulomatous disorders such as sarcoidosis,
Transfusion reaction 
Drug-related fever 
Amphotericin B, beta-lactams (penicillins, cephalosporins), sulfonamides, carbamazepine, phenytoin, procainamide, quinidine, hydralazine, interferon-alpha, interleukin-2.
.►Tissue damage (e.g postoperative fever, myocardial infarction, hematoma)

►Thromboembolism (acute thrombophlebitis, pulmonary embolism)
►Neurologic causes 
(intracranial hemorrhage, cerebrovascular accident, malignant neuroleptic syndrome).
►Endocrine causes (thyroid storm)

Causes of fever to be treated in an emergency basis

The physician should be alert to quickly diagnose and treat any of the following causes of fever, which may pose significant risks to the patient and are generally considered as emergencies or as serious diseases.

Systemic conditions: 

sepsis-septic shock (see the chapter on shock Shock: diagnosis and treatment)

menigococcemia

From the central nervous system

meningitis (for its diagnosis and treatment click Meningitis)

encephalitis

cavernous sinus thrombosis

 brain abscess

From the respiratory system

pneumonia (which may in some cases cause respiratory failure), 

(For pneumonia diagnosis and treatment click Pneumonia )

epiglottitis

peritonsillar abscess

retropharyngeal abscess

From the cardiovascular system

infective endocarditis

pericarditis 

From the gastrointestinal system

peritonitis 

cholecystitis

appendicitis

diverticulitis

intra-abdominal abscess

From the genitourinary system

pyelonephritis

 tubo-ovarian abscess

pelvic inflammatory disease

From the skin and soft tissues

cellulitis,

 infected decubitus ulcer

 soft tissue abscess

From the skeletal system

osteomyelitis

The history of the patient with fever

It is important to determine if there are any associated symptoms and also if the onset of fever occurred in the hospital (suggestive of a nosocomial infection) or in the community. Associated symptoms can point toward the probable causes and guide subsequent diagnostic tests if necessary. The symptoms to ascertain include chills, rigors, night sweats, rash, arthralgias, myalgias, sore throat, cough, sputum production, postnasal drainage, dysuria (painful urination), urinary frequency (more frequent urination than normal e.g. every 1-2 hours), headache, facial pain, chest pain, abdominal pain, nausea, vomiting, diarrhea, pain at an intravenous site, and change in mental status. A rigor (shaking chill), suggests a bacterial infection (e.g. pneumonia, pyelonephritis, bacteremia, or sepsis ).

The history of any medical illnesses and surgeries, as well as any medications that the patient regularly takes,  is important. Information should be obtained whether a condition that can reduce the function of the patient's immune system is present because such conditions predispose to infections with certain microorganisms. For example, a history of splenectomy (usually due to splenic rupture as a result of trauma) carries a higher risk of infection with encapsulated microorganisms such as Streptococcus pneumoniae. An underlying malignancy, chemotherapy, other immunosuppressive medications (such as prednisone or azathioprine), or neutropenia, or AIDS (acquired immunodeficiency syndrome due to HIV virus infection) also place the patient at increased risk of infection and often with less common causal microorganisms (opportunistic infection).

There are also other conditions from the medical history which are important because they may predispose to specific infections, e.g. a prosthetic heart valve or a congenital heart defect can predispose to endocarditis, chronic obstructive pulmonary disease (COPD) which is usually the result of heavy smoking may predispose to a lower respiratory tract infection, renal calculi, anatomical or functional abnormalities of the urinary tract or pregnancy may predispose to pyelonephritis, patients with cholelithiasis or obese middle-aged or older females are at a higher risk for cholecystitis, chronic liver disease predisposes to spontaneous bacterial peritonitis, pneumococcal pneumonia or bacteremia, etc.
It is also important to consider if iatrogenic predisposing factors or causes of infection are present e.g. peripheral or central intravenous catheters can become infected, a nasogastric tube may predispose to sinusitis. a Foley catheter can predispose to a urinary tract infection, devices such as pacemakers and their leads can be infected, endotracheal intubation may predispose to a pulmonary infection, recent surgery can be complicated by infection of the wound, or infection of a prosthetic material recently placed, etc.

Physical examination of the patient with fever

 General appearance: Does the patient appear toxic, in a severe condition, or does he or she look relatively well? This can help decide whether the patient should be treated with empiric antibiotic therapy, before definitive diagnosis, based on the most likely cause.
A rigor (shaking chill), suggests a bacterial infection (e.g. pneumonia, pyelonephritis, bacteremia, or sepsis ). Vital signs: 
Oral and rectal temperature should be taken. (Known neutropenia is a contraindication to taking rectal temperature).
Pulse and blood pressure: It is very important to know if the patient is hemodynamically stable. Hypotension (systolic blood pressure < 100 mmHg) suggests sepsis or volume depletion.
As a general rule, the heart rate of a febrile patient is expected to be elevated, depending on body temperature.
If the heart rate is not elevated as expected by the level of fever (pulse-temperature dissociation), this may result from beta-blocker treatment or from certain specific causes of fever such as brucellosis, typhoid fever (Salmonella typhi), atypical pneumonia (pulmonary infection from Mycoplasma or Chlamydia pneumoniae or Legionella pneumophila), Psittacosis (infection by Chlamydia psittaci), malaria, drug-related fever, lymphoma, or fever due to central nervous system disorder. 
 Examination of the skin and inspection of the patient:
 Check for an area of focal erythema (suggesting an infection of the skin) or focal edema and erythema at sites of intravenous catheters, if any. In febrile patients with any type of catheter (e.g. an intravenous catheter or a Foley catheter) assume that fever is due to a catheter-related infection unless proved otherwise. Inspect the skin for rashes (in some cases the specific appearance of the rash may suggest the diagnosis). Pustules can be found in staphylococcal disease and gonococcemia. (Pustules are small circumscribed elevations of the skin containing pus and having an inflamed base).
Look for signs that may suggest infective endocarditis such as painful erythematous subcutaneous nodules on the tips of digits (Osler nodes), non-tender hemorrhagic macules on the palms or soles (Janeway lesions), petechiae, and splinter hemorrhages under the nails.

Purpuric rash of meningococcemia (bacteremia caused by fulminant infection by Neisseria Meningitidis) in a 15 year old girl . The girl was succesfully treated with intravenous ceftriaxone.Figure available via creative commons licence CC BY-NC 4.0 From Researchgate.net LINK  https://www.researchgate.net/figure/Purpuric-rash-of-meningococcemia-at-presentationReprinted-with-permission-from-The_fig1_255959317  From the article : Shrestha P, Shrestha NK, Giri S.  Rapid recovery following fulminant meningococcemia complicated by myocarditis in a 15-year-old Nepalese girl: a case report. International medical case reports journal. 2013 6. 33-6. 10.2147/IMCRJ.S36713. https://www.dovepress.com/rapid-recovery-following-fulminant-meningococcemia-complicated-by-myoc-peer-reviewed-article-IMCRJ

HEENT examination
Check for evidence of bacterial tonsilitis (red swollen tonsils with white spots and swollen uvula). In viral pharyngitis /tonsilitis tonsils will also be red and swollen but without white spots of pus and without a swollen uvula. Percuss the teeth for tenderness (suggesting an abscess). Percuss the paranasal sinuses for tenderness, suggestive of sinusitis. Examine the tympanic membranes with an otoscope for evidence of otitis media.
Lymph nodes
Check for enlarged lymph nodes (cervical, supraclavicular, epitrochlear, axillary, and inguinal nodes). In adults, nodes larger than 1 cm in diameter are often pathologic. Focal adenopathy may suggest the location of a bacterial infection in a territory drained by the affected lymph nodes, e.g. group A streptococcal pharyngitis classically can cause anterior cervical lymphadenopathy(with fever and a sore throat), whereas an infection of the hand may cause axillary lymphadenopathy. Note that most children normally have palpable anterior cervical, inguinal, and axillary lymph nodes that, if evaluated by adult standards, would be characterized as lymphadenopathy. Lymphoid mass gradually increases after birth until the age of 8-11 years and then it undergoes progressive atrophy during puberty. In young children, anterior cervical lymph nodes as large as 2 cm, inguinal lymph nodes as large as 1.5 cm and axillary nodes as large as 1 cm in diameter, are usually normal.

Diagnostic tests

Diagnostic tests are an adjunct to the history and the physical examination and they are selected according to the history and the findings of the physical examination.
Complete blood count (CBC)
An elevated number of white blood cells (WBC) is often associated with infection, though some viral infections are associated with
leukopenia (a reduced number of WBC). Bacterial infections are usually associated with an increase in polymorphonuclear neutrophils, often with an elevated number of earlier developmental forms such as bands. Viral infections usually demonstrate an increase in lymphocytes. Infections from some parasites demonstrate an increase in eosinophils.
Inflammatory Markers
The erythrocyte sedimentation rate (ESR) and the C-reactive protein (CRP) level rise in inflammation and they are used to assess a patient's level (severity/intensity) of inflammation. They are sensitive markers of inflammation but they are nonspecific tests regarding the cause and site of inflammation. CRP changes more rapidly in response to changes in the intensity of the inflammatory process (even in 24 hours) whereas  ESR changes slowly (in several days) therefore it is usually not useful to measure it more often than weekly.
Based on clinical suspicion serologic and antigen tests for specific pathogens can be ordered.
Cultures:
 For the diagnosis of infectious disease and for the identification of the microorganism and its sensitivity to drug treatment cultures are very helpful. Cultures involve the culture of fluid (e.g., blood, urine, sputum, pus from a wound) or the culture of infected
tissue (e.g., surgical specimens). Samples can be sent for culture of bacteria (aerobic or anaerobic), fungi, or viruses.
Analysis of cerebrospinal fluid (CSF) is indicated in patients with suspected meningitis or encephalitis.

Sepsis

Sepsis is a clinical syndrome that occurs in patients with infection (known or suspected) having indications of a systemic inflammatory response. According to a more recent task force definition sepsis is a clinical syndrome characterized by the presence of a life-threatening organ dysfunction caused by a dysregulated host response to infection.  Sepsis is a life-threatening condition, therefore early diagnosis is required and prompt treatment with intravenous empirical antibiotics.
 Sepsis can be defined as an infection that fulfills  two or more criteria of the systemic inflammatory response syndrome (SIRS), These criteria include:

• Fever or hypothermia (temperature  >38° C (>100.4 °F)  or < 36° C ( < 96.8°F)
• Resting respiratory rate >20/ minute (tachypnea)
• Resting heart rate (HR) >90 beats per minute (bpm)
• Altered mental status
• White blood cell count (WBC) elevated >12,000 or reduced <4,000 / or 10% bands
• Hyperglycemia (in a nondiabetic patient)

However, the SIRS criteria although sensitive to detect sepsis had a relatively low specificity since similar inflammatory responses can be seen as a response to non-infectious conditions (for example surgery, pancreatitis, etc). Furthermore, the SIRS criteria do not perform well in identifying patients with significant morbidity and mortality who need intensive treatment, probably in an ICU (intensive care unit).
These issues have led to a recent new consensus definition for sepsis in 2016. The international task force defined sepsis as a life-threatening organ dysfunction caused by a dysregulated host response to infection.

Patients with sepsis can also be identified using the qSOFA score which was developed by an international task force. A patient suspected to have an infection that fulfills two of the following criteria should be treated as a patient with sepsis:
qSOFA criteria

•  Respiratory rate ≥22/min
•  Glasgow Coma Scale <15
•  Systolic blood pressure ≤100 mmHg

Severe sepsis is a clinical syndrome of sepsis that is associated with at least one new organ dysfunction. The presence of at least one of the following findings in a patient with sepsis is indicative of severe sepsis:

• Systolic blood pressure (SBP) <90 mmHg or mean arterial pressure (MAP) <60 mmHg, 
• Change in mental status, delirium
• Indications of reduced peripheral tissue perfusion, such as  poor extremity perfusion (cool extremities, livedo reticularis) or lactic acidosis (2.0–4.0 mM/L) (mM/L= millimole per liter)
• New renal dysfunction: Increased creatinine (>2.0 mg/dl or increase in creatinine by 50%) or oliguria
• New respiratory dysfunction: Hypoxia or high FiO2 requirement
• Abnormal prothrombin time/partial thromboplastin time (PT/PTT) or low platelets (<100,000)
• New hepatic dysfunction: Hyperbilirubinemia (>2.0 mg/dl) or liver function tests > twice the upper limit of normal

Septic shock is a subcategory of severe sepsis characterized by severe circulatory dysfunction due to an infection, as defined by hypotension (systolic BP <90 mmHg or 40 mm Hg less than baseline) in the presence of evidence of hypoperfusion, despite an intravenous fluid challenge of at least 20 mL/kg.

Criteria for septic shock

•  A need for vasopressor therapy to maintain a mean arterial pressure ≥ 65 mmHg
•  Serum lactate > 2 mM/L which persists after adequate fluid resuscitation

Cryptic septic shock is a new term indicating circulatory dysfunction due to sepsis but without hypotension. Cryptic septic shock is defined as sepsis with severe lactic acidosis (4.0 mM/L or greater) despite a normal or high blood pressure.

Management of sepsis

If the patient has hypoxemia administer adequate oxygen
to maintain arterial hemoglobin oxygen saturation > 95% .
Intravenous saline is administered to all patients with sepsis.
For patients with hypotension, this should be a bolus of 500 mL of saline over 15 minutes. Further fluid administration should be titrated according to the response. To maintain fluid balance urine output and all fluids administered should be recorded. Early goal-directed therapy:
Usually, 500 ml boluses of 0.9% saline up to 1-2 L are empirically administered. Persistent hypotension despite adequate intravenous fluid administration usually requires admission to an ICU and the use of vasopressors. In this case, norepinephrine (noradrenaline) is the preferred drug.
It is helpful to place a central venous line, in order to measure the central venous pressure (CVP). The CVP can be used as a guide for fluid administration. Boluses of 500 ml saline should be administered until CVP >8 cm H₂O .
If the mean arterial pressure <65 mm Hg and CVP >8, then initiate
the intravenous administration of vasopressors, such as norepinephrine (2-8 μg/min) or dopamine (the pressor dose of dopamine is 5-10 μg/kg/min)  to raise blood pressure. ( μg= microgram)
Generally, norepinephrine is preferred, especially if tachycardia or arrhythmias are present.

Prompt and appropriate antimicrobial therapy must be administered as quickly as possible with wide-spectrum intravenous antimicrobials that target the likely causative microorganisms. Such drugs should be given quickly, ideally within 1 hour of admission. Prior to the administration of antibiotics, blood cultures should be taken.
In a patient with sepsis with normal immune function without an identifiable source of infection the initial empirical antibiotic treatment consists of :
Second or third-generation cephalosporin plus gentamicin, or
vancomycin plus third or fourth generation cephalosporin, or
Nafcillin and gentamicin, or
If the patient resides in a nursing facility, or there is a history of recent hospitalizations or a history of methicillin-resistant Staphylococcus aureus then vancomycin should be added to the above antibiotic treatment.
Sepsis in an immunocompromised patient without an identifiable source of infection is treated with:
Piperacillin and gentamicin
Ceftazidime and either nafcillin or vancomycin and gentamicin.
Empiric antibiotic therapy in pediatric patients with sepsis:
Neonates: Ampicillin plus cefotaxime.

Children: Vancomycin plus cefotaxime.

If the source of infection has been identified, or highly suspected, the empirical broad-spectrum antibiotic regimen should be especially effective for  the most likely organisms:
Pulmonary source:
Second or third-generation cephalosporin and gentamicin
Intra-abdominal source:
Ampicillin plus metronidazole plus gentamicin or
Cefoxitin plus gentamicin
Urinary tract source:

Ampicillin or piperacillin plus gentamicin or levofloxacin
Dosage of intravenous (IV) antibiotics:
Ampicillin: 1-2 g (pediatric: 50-200 mg/kg/24 h) IV q 4-6 h
(q 4-6 h= given every 4-6 hours)
Cefoxitin: 1-2 g (pediatric: 100-160 mg/kg/24 h) IV q 6-8 h
Ceftazidime: 1-2 g (pediatric: 100-150 mg/kg/24 h) IV q 8-12 h
Gentamicin: 1-1.5 mg/kg (pediatric: 2-2.5 mg/kg q 8 h) IV q 8h
Metronidazole: Load with 1 g (pediatric: 15 mg/kg) IV, then 500 mg (peds: 7.5 mg/kg) q 6 h
Nafcillin: 1-2 g IV q 4 h (pediatric: 50 mg/kg/24 h divided in  4-6 hour dosing intervals)
Norepinephrine: 2-8 μg/min
Piperacillin: 3- 4 g IV q4–6h
Vancomycin: 500 mg (pediatric: 10 mg/kg) IV q 6 h

It is also very important to identify the likely source of infection from the history, clinical examination and appropriate radiological and laboratory tests. If a specific source of infection is identified its prompt management is vital, for example, debridement of an infected wound, drainage of an infectious pleural effusion (empyema), or surgery to drain an intra-abdominal abscess or to cure another local focus of infection, if present.

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LINK: Emergency medicine book-Table of contents

Bibliography

The patient with fever  (a powerpoint presentation-PPT- by Dr Förhécz Zsolt

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 Fever, In Haist SA Robbins JB, Gomella LG (eds.) Internal Medicine on call 4th edition  2015 Mc Graw Hill pp.133-141

Acute fever Wiki EM

Fever and infectious disease-MSD manual

DeWitt S, Chavez SA, Perkins J, Long B, Koyfman A. Evaluation of fever in the emergency department. Am J Emerg Med. 2017 Nov;35(11):1755-1758. 

Hersch EC, Oh RC. Prolonged Febrile Illness and Fever of Unknown Origin in Adults. Am Fam Physician. 2014;90(2):91-96.
LINK Prolonged Febrile Illness and Fever of Unknown Origin in Adults

Fever of unknown origin-clinical advisor decision support in medicine

Evans, T. Diagnosis and management of sepsis. Clinical Medicine 2018;18(2): 146–149.doi:10.7861/clinmedicine.18-2-146
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Sepsis and septic shock-Clinical advisor -decision support in medicine