VIMS Journal: December 2016

Review Article

Oxygen Therapy

Dr. Tulsi Nag

Abstract :
Oxygen is an atmospheric gas essential forsurvival of all living things. Presence of "air",vital for survival of human was recognised inthe ancient Greek, as well as in Vedic Hinduliterature, more than 2000yrs ago. But it wasonly in the 18th century that that gas was isolatedby Joseph Priesley and its importance inrespiratory physiology was described by AntoineLavoisier.

Oxygen is considered as the first line drugrequired for the management of hypoxaemia andseveral other diseases characterized by hypoxicconditions. It is therefore used for a large numberof pulmonary and non-pulmonary diseases forits definitive, supplementary or palliative role.

Goal of oxygen therapy is to -
1) Relieve hypoxaemia and hypoxia.
2) Maintain adequate oxygen delivery to thetissues by increasing alveolar oxygen tension.
Oxygen is used liberally in ICU patients to correcthypoxaemia to >60mmHg or SaO2>90%.

Oxygen therapy requires hourly assessment ofSPO2 from continuous pulse oximetry, Heartrate, Respiratory rate, Respiratory effect, Colour,Level of Consciousness, Oxygen flow rate.

In correct situations oxygen is a life saving drugand therapy. It remains a part of initialresuscitation and ongoing management ofcritically unwell.

However, oxygen may have detrimental effects in certain patients and/or certain situations.
In contrary to popular perception that oxygenprotects cells from injury in critically ill patients,evidences indicate that oxygen is the source ofcell injury via toxic metabolites in criticallyunwell, if not administered correctly. Generalpatients should remain below an FiO2 of 0.5and the period should be kept to the minimumrequired (not more than 48 hours).

Keywords :
Oxygen, Hypoxaemia, Humidification, Deliverydevices.

Inroduction :
Oxygen is an atmospheric gas essential forsurvival of all living things. Presence of "air",vital for survival of human was recognised inthe ancient Greek, as well as in Vedic Hinduliterature, more than 2000yrs ago. But it wasonly in the 18th century that that gas was isolatedby Joseph Priesley and its importance inrespiratory physiology was described by AntoineLavoisier. Rapid development took place in thesubsequent years. The problems of oxygendeficiency as well as the need and indicationsfor oxygen therapy were subsequentlyrecognized. Soon oxygen came to be known as"cure all medicine" used for conditions varyingfrom cholera, arthritis, anaemia and syphilis toglaucoma, epilepsy, diabetes and cancer. It wasaround second decade of 20th century and laterthat the oxygen therapy was adopted forindications based on firm scientific foundation.

Hypoxaemia and Hypoxia :
Oxygen is considered as first line drug requiredfor management of hypoxaemia and several otherdiseases characterized by hypoxic conditions. Itis therefore used for a large number of pulmonaryand non pulmonary diseases for its definitive,supplementary or palliative role.

Hypoxiaemia is low arterial oxygentension(PaO2) below the normal level (less than60mmHg).

Cases of Hypoxiaemia:
- Reduced inspired oxygen tension(highaltitude).
- Hypoventilation
- VA/Q mismatch
- Right to left shunt
- Diffusion defect at gas exchange level.

Hypoxia is defined as the lack of oxygen at tissuelevel which can lead to changes in function,metabolism or even structure of the body.

Types of hypoxia
Hypoxia is classified as hypoxaemic ornormoxaemic categories based on PaO2 levels.
A)Hypoxic hypoxia
Oxygen deficiency results when oxygentension in arterial blood is low. PaO2 isdecreased as in low environmental oxygenventilator failure pulmonary shunt.
B)Normoxaemic hypoxia
It is tissue hypoxia in absence of low PaO2.It is difficult to measure quantiaatively butis diagnosed from the clinical features andlaboratory parameters. It develops when tissuedemands for oxygen are not supplied by theavailable oxygen stores. This includes:

a) Circulatory or stagnant hypoxia which resultsfrom an inadequate supply of oxygenated bloodto the tissues when the blood flow is eitherdecreased as in Cardiac failure, hypovolaemiaand shock or when blood flow is altered due toexcessive PEEP during mechanical ventilation
- Sepsis
- Abnormal body temperature
- Thyroid dysfunction
- PaO2 is normal and PvO2 is decreased.
- Blood flow is insufficient.

b) Anaemic hypoxia occurs due to deficiencyof haemoglobin or an altered affinity ofhaemoglobin to oxygen as seen in -
- Severe anaemia
- Haemorhage
- CO poisoning
- Methaemoglobinemia
- Haemoglobinopathies

Oxygen content is decreased. PaO2 is normal.PVO2 is decreased due to prolonged extractionby tissues.

c) Histotoxic hypoxia results from failure ofcellular metabolism in cases of tissue poisoningby toxic agents -
Cyanide poisoning
Septic Shock

Some other systemic diseases cells can not utilizeoxygen as electron transfer system of cytochromeoxidase is paralysed. PaO2 is normal. PVO2 isincreased as O2 is not extracted from blood.
Hypoxia can also result when the demand foror utilization of oxygen by the tissues is increasedeven though oxygen delivery is normal or increased. This occurs during excessive stresssuch as
- Hyperpyrexia
- Thyrotoxicosis
- Other hyper metabolic situations.

Oxygen Therapy:
Oxygen is used as therapy in most critically illpatients in I.C.U. Goal of oxygen therapy is i)To relieve hypoxaemia / hypoxia, ii) To maintainadequate oxygen delivery to the tissuesby increasing alveolar oxygen tension.Oxygen is used liberally in ICU patients tocorrect hypoxaemia to a PaO2>60mmmkg orSaO2>90%.
Dramatic improvement with oxygen therapyoccurs when arterial with oxygen therapy occurswhen arterial hypoxaemia (low PaO2) is due tolow PAO2 or V/Q mismatch. Relief of hypoxiain such patients bring 3 effects i) decreased workof breathing, ii) Decreased myocardial stress andiii) Improved cell function.

A. Indications of oxygen therapy

1. Hypoxaemia -
- Cardiopulmonary or respiratory arrest.
- Hypoventilation from any cause.
- Respiratory disease characterized by V/Qmismatch with or without impaireddiffusion across alveolar capillarymembrane.
- Heart failure
- Pneumonia
- Pulmonary embolism
- Shock.

2. Respiratory distress with respiratory ratemore than 24/min.

Pneumothorax - Oxygen increases rate ofresolution.

Myocardial infarction and unstable angina.

Acute respiratory failure (hypoxaemic andhypercapnic)

Hypoxia due to decreased transportation ofoxygen with impaired perfusion of tissues-
- Shock from any cause
- Left Ventricular failure
- Cardiac arrhythmias causing haemodynamicinstability.
- Cardiac arrest.

Hypoxia due to poor uptake or utilizationof oxygen in tissues.

Abnormalities in quantity, quality & type ofhaemoglobin -
- Acute blood losss
- Severe anaemia
- Methaemoglobinemia
- Co poisoning

During increased demand as in -
- Shivering
- Hyperthroidism
- Hyperthermia
- Preoxygenation before induction
- At high altitude

Acute asthma

Preoperative and post operative state.

Low cardiac output and metabolic acidosis.

Surgical indications of oxygen therapy
Abnormalities of gas exchange are present bothduring surgery and in post-operative period.Hypoxaemia with or without Co2 refeution mayoccur because of problems of V/Q relationshipand/or hypoventilation. Oxygen administrationalong with other treatment is required in all suchpatients with complications.
Post operative states
Mild to moderate hypoxaemia is common in firstfew hours after general anaesthesia speciallyafter abdominal and thoracic surgeries due tomaldistribution of ventilation and increasedphysiological shunt.
Central and peripheral depression of ventilationdue to residual effects of anaestheties and opioidanalgesies.
Shivering after anaesthesia and some degree ofdiffusion defects can lead to hypoxaemia whichmay be serious in presence of preexisting riskfactors or low PaO2 . Such patients require oxygentherapy for several hours depending on PaO2 level and other clinical parameters.
All such patients are given oxygen until fullyawake and vital signs are normal and stable.Most patients require only small increase in FiO2 adminstered via nasal cannula at a flow rate of5-6L/min.
In patients with significant cardiopulmonarydisease and after pulmonary or cardiothoracicsurgery oxygen is continued until ABG analysisindicates that oxygen is not required.

A. Monitoring of oxygen therapyOxygen therapy requires :-
1) hourly assessment of SpO2from continuouspulse oximetry.
2) Heart rate
3) Respiratory rate
4) Respiratory effort
5) Colour
6) Levels of responsiveness
7) Oxygen flow (temperature if included)
It also requires hourly documentation of
- Indication
- Made of delivery
- Device used
- FiO2and /or liter flow
- SpO2

B. Humidification
One of the complications of oxygen therapyeven for a short period of time, is the drying ofupper airway which causes secretions to bethicker and harder to expectorate. If there is notenough humidity in inspired gas, not only thenasal passages become dry and painful, there isa higher risk of development of atelactasis, lungcollapse or infection. So consideration shouldbe given to humidification of oxygen.Humidification minimizes the inflammation,mucosal drying and retention of secretion.Oxygen is to be humidified for the comfort ofthe patients.
Humidification is usually not required if thepatient is on low flow oxygen for short term.Humidification should be considered if theoxygen is required for longer than 48 hrs or ifnasal passages become uncomfortable or dry.

C. Weaning
Oxygen should be stopped arterial oxygenationis adequate with the patient breathing room air(PaO2>60mmHg and SaO2>90%. In patientswithout hypoxaemia but at risk of tissue hypoxia,oxygen should be stopped when the acid-basestatus and clinical assessment of vital organ functions are consistent with resolution of tissuehypoxia. Weaning should be initiated once thepatient's underlying disease process is stabilizedand bed side evaluation of respiratory rate, heartrate, blood pressure, skin colour and pulseoximetry are normal and patient is comfortable.Wearing should be gradually attempted bylowering the concentration for a fixed period andre-evaluating the clinical parameters and SpO2.An initial withdrawl for about 30min is followedby longer periods. It no deterioration oxygenmay be completely withdrawn. If patient's heartrate and/or respiratory rate increase by 20%,oxygen flow is to be increased.
In patients with underlying chronic respiratorydisease, oxygen may be required at a lowerconcentration for longer period.

D. Complications of oxygen therapy
In correct situation oxygen is a life savingdrug/therapy. It remains a part of initialresuscitation and ongoing management ofcritically unwell.
However, oxygen may have detrimental effectsin certain patients and/or certain situations.In contrary to popular perception that oxygenprotects cells from injury in critically ill patients, evidences indicate that oxygen is the source ofcell injury. Via toxic metatobiles in critically illpatients, if not administered correctly. Generallypatients should remain below an FiO2 of 0.5 andthe period should be kept to the minimumrequired (not more than 48hrs).

1. Fire- Oxygen is supplied as compressed gasin cylinders and pipe line. So there remains riskof explosion.

Though oxygen does not itself explode or burn,it supports combustion and enhances theinflammable properties of grease and oil. Thereis also small risk of fire if dirt, grease, oilcontaminate connects between medical devicesand gas cylinders.

Facial burns may occur in patients who smokewhile using oxygen therapy.

As oxygen is supplied as compressed gas, thereremains chance of barotrauma to airway andalveoli, if its administration is not governed byflow meter (pressure limiting valve).
2. Patient related :
a) Loss of hypoxic drive -
Both elevated blood PaO2 and decreased bloodPH are strong stimulant to respiration. Patientswith chronic lung disease with CO2 retensionfor some time become used to high CO2 leveland rely on decreased oxygen level in blood fortheir respiratory drive.

Administration of oxygen above 24% in thesepatients may abolish the hypoxic drive torespiration leading to further CO2 refeusion andrespiratory arrest (CO2 narcosis).
b) Drying and crusting of secretions in respiratorytract occurs after use of unhumidified oxygenleading to blockage of bronchi by inspiratedmucus and complete or partial blockage ofartificial airways. There may be decreasedmucociliary clearance & tracheobronchitis.
c) Oxygen toxicity
Oxygen is considered as pharmacotherapy inmedical environment and as with all drugs ithas side effects in overdose. The metabolytesof oxygen are more damaging than parentmolecul and can inflict lethal injury.
Lung toxicity (Lorriance Smith effect) -
Exposure to high FiO2 for a prolonged period results in pulmonary injury. It involves directcellular damage to lung tissue by highly reactiveoxygen free radical. High concentration of oxygen(more than 60%) may damage alveolar membranewhen inhaled for 18 hours. Progression to ARDSwith high protein alveolar oedema and pulmonaryradiographic infiltrate is associated with highmortality. CNS toxicity (Paul Bert effect) -
oxygen delivery at higher pressure (> 3atmosphere) can lead to acute CNS signs andseizures. It is best avoided by restricting deliveryof oxygen to the lowest concentration and shortestduration absolutely necessary to achieve asatisfactory PaO2.

d) Other pulmonary effects
Supplemental oxygen also have otherphysiological effects within the which are nottoxic but cause problems in themselves:
i) V/Q mismatch - high concentration ofinspired oxygen decreases effect of HPV,diverting the blood through poorly ventilatedlung with increased shunt and decreased PaO2.
ii) Haldane effect - Increasing FiO2 decreasesCo2 duffering capacity of haemoglobin, leadingto increased PaCO2 and acidimia.
iii) Absorption atelectasis - in presence of smallairway obstruction high alveolar oxygenconcentration leads to rapid absorption of gascausing collapse of alveoli and decreaseddiffusion surface area, even at an FiO2 of 0.5.
iv) Increased work of breathing - as oxygen ismore dense than air, breathing high concentrationat increased viscosity causes increased work ofbreathing which is more significant in patientswith chronic lung disease.

e) Vasoconstriction
Oxygen causes constriction of coronary, cerebraland renal vasculature leading to hypoperfusionof key organ systems -potentially reducing DO2when an increase is desired.
Hyperoxia decreases cerebral blood flowsignificantly resulting a worse outcome followinga mild to moderate cerebrovascular accident.
Coronary blood flow is also decreased inpresence of hyperoxaemia promoting myocardialischaemia during acute coronary syndrome. Sothe recommendation is not to give supplementaloxygen to patients with acute chest pain withoutevidence of hypoxaemia.

f) Danger of oxygen withdrawlOxygen is indicated needs to be givencontinuously till hypoxia is releaved. Intermittentoxygen therapy can be dangerous in hypoxicpatients. It only provides period of relief fromhypoxia followed by periods of worsening andoften extreme hypoxia.

Hyperbaric oxygen therapy
Here oxygen is delivered to the patient at apressure higher than atmospherie pressure (2-3 atmosphere). Hyperbaric oxygen therapy isdelivered either in a monoplace chamberdesigned for one individual or in a multiplacechamber for 2 or 3 people. The chamberencompasses the whole body and the gas ispiped from sources, heated and humidified.Indications for hyperbaric oxygen therapyThere are very few indications for increasingPaO2 above normal (100mmHg). Indeed it isharmful.
A. Primary therapy
Carbon monoxide poisoning (copoisoning)
Air or gas embolism
Decompression sickness
Clostidial myositis and myonecrosis clusterheadache.
Carbon monoxide binds to haemoglobin with anaffinity 210 times that of oxygen.So copoisoningnecessitate hyperoxic therapy. Factors such asincreased age (>35yrs), an exposure of morethan 24hrs, an associated loss of consciousnessand carboxyhaemoglobin levels >25% appearsto result in an increased incidence of neurologicalsequale and probably benefit from hyperbaricoxygen.

B. Adjunctive therapy
Radiation tissue damage.
Crush injuries
Compromised skin flaps or grafts
Refractory osteomyelitis.
Intracranial abscess
Chronic wound healing
Complication of hyperbaric oxygen therapy
1. Barotrauma - Middle ear and sinuses
Rupture of oval or round window
G.I. distenssion
Tooth displacement and pain
Gasembolism on decompensation .
1. Oxygen toxicity - (as above) specially aproblem in the critically ill who may be onhigh concentration for longer period.
2. Generalized seizures - Paul Bert effect
3. Visual problems - Acute myopia
Cataract formation.

Oxygen therapy apparatus and devices :In the hypoxic self ventilating patients deliveryof oxygen to the alveoli is usually achieved byincreasing the inspired Oxygen fraction (FiO2).Non-invasive devices for delivering oxygenconscious patients can broadly be divided intofour categories :
1. Variable performance devices
2. Fixed performance devices
3. High flow systems
4. Others - oxygen tent
oxygen hood
extra corporeal membrane oxygenation (ECMO)
5. Blow over oxygen
6. Oxygen conserving devices

I. Variable performance devices
These devices cannot deliver a fixedpercentage of oxygen ( FiO2). The gas flow isinsufficient to meet patient's peak inspiratoryand minute ventilation requirement. They deliverlow to moderate and variable FiO2. FiO2depends on patient's respiratory rate and tidalvolume. They include -
Nasal cannulae/nasal prongs.
Face masks
Tracheostomy mask
Head box
A. Nasal Cannulae / Nasal prongs
Available in single or double cannulae. Thelatter is most commonly used.
Lost Cost, safe, simple and comfortable for longperiod.
Prevent rebreathing of CO2. Effective fordelivering low concentration of oxygen between24% & 35%. Concentration of oxygen delivereddepends on flow rate (1-4L/min).

B. Face mask
Face mask is applied over the mouth and nose.This increases the size of the reservoir, so thata higher flow rate can be administered.
i) Simple face mask
Variable performance device
Reservoir is 100-200ml
FiO2 varies with -
- Oxygen input flow
- Mask volume
- Patient's breathing pattern
FiO2 – 40-60%
Input flow range is 5-10L/min
Minimum gas flow of 5L/min must be maintainedto prevent rebreathing.
The vent holes in the mask allows room air tobe inspired in addition to the oxygen to bedelivered and exhaled CO2 to be released .
ii) Non-rebreathing mask (Trauma fask)
- Variable performance device.
- Reservoir volume is 600-1000ml
- FiO2 - 60-80%
- Input flow range -10-15L/min
Factors affecting FiO2 -
- Air leakage
- Patient's breathing patternThe expiratory port on the mask are covered withflaps that allow exhaled gas to escape but preventthe inhalation of room air. There is also one wayvalve between reservoir bag and mask that allowsinhalation of gas from the bag but prevent exhaledgas entering the bag. Bag should be 1/3 to ½full at all times.

iii)Partial rebreathing mask
Flow rate ->10L/min
Reservoir volume - 600-1000ml
FiO2 range - 40-70%, Input flowrange>7L/min
Variable performance device.
The bag should remain inflated to ensure thehighest FiO2 and to prevent excessiverebreathing.

A)Tracheostomy mask
Semi rigid plastic masks. Act in same way asfacial masks. A variable performance device,used primarily to deliver humidity to patientwith artificial airways. The delivery they achieveis dependent on the presence of an endotrachealtube & inflation status of the cuff. Used inpatients having tracheostomy or laryngectomy.
B) Head box
May be considered for infants if higher oxygenconcentration with humidification is required.It also facilitates the observation of work ofbreathing.

II. Fixed performance devices
These devices deliver a known percentage ofoxygen by mixing oxygen and air via venturidevice. Their delivery of oxygen is independentof patients factors
They include -
- Venturimasks and adapters
- Anaesthetic breathing circuit
- T-piece system
a) Venturi masks and adaptors
The venturi mask contains a differing size holes situated at the base of the mask containing venturivalves which use principle of jet mixing(Bernoulli effect). When oxygen passes throughthe narrow orifice, it produces a high velocitystream that drawn a constant proportion of roomair (upto 40L) through base of the venturi valves.Air entrainment depends on -
Velocity of the jet (size of the orifice and oxygenflow rate) and size of valve ports. Each diameterof the venturi valve gives a different final oxygenconcentration and are available to give aconcentration of 24-60%. Each concentrationneeds a different oxygen flow setting. Ability todeliver a constant FiO2, which is desirable inpatients with chronic CO2 refention (type IIrespiratory failure).
FiO2 - Colour coded jets are attached to maskto deliver desired concentration of oxygen. Blue- 24%; Yellow - 28%; White - 31%; Green -35%; Pink - 40%; Orange - 50%. (Colour andpercentage can change between differentmanufacturers). Product information on Packshould be checked while using.
Flow rate - 12-15L/min. Requires a miximumflow rate of about 5L/min and is dependent onthe oxygen concentration required.

b) Anaesthetic breathing circuits
Non-rebreathing systems have one-way valve(Ambu bag) and is usually closed mask systems,so they deliver the set concentration.
Non-rebreathing systems (Mapleson'sA,B,C,D,E) depend on gas flow to ensure norebreathing (most require flows>150ml/kg). Noentrainment is possible. Rebreathing occursreadily at low flows.
In cardiac or respiratory arrest, tight fittinganaesthetic type mask can achieve 100% oxygen.

c) T-piece system -
It has an inspiratory and an expiratory limbforming the bar of T. it can be used withendotracheal tubes (oral, nasal andthacheostomy) or with a sealed CPAP type mask.The T-piece can act as a fixed performancesystem if oxygen flow rate is sufficiently high.Oxygen flow rates need to be high enough toprevent rebreathing of expired gas andentrainment of room air air.

III. Humidified High Flow Nasal Cannula(HHFNC)
Air oxygen blendder. Requires a flow rate of60L/min. Delivers FiO2 of 21-100%. HHFNCis a system having ability to provide humidifiedand heated high flow mixture of air and oxygenvia a specialized nasal cannula. As the inspiredgas is warmed and humidified it is better toleratedby patients. It is able to deliver PEEP ofapproximately 4-8 cm H2O.
Aim of HHFNC is to decrease work of breathingto a respiratory rate < 25/min and SaO2>90%.
The advantage include improved oxygenationand gas exchange avoiding intubation andmechanical ventilation in patients refractory tohypoxaemia. In patients with respiratory failureHHFNC oxygen delivery system is an alternativeto low flow mask oxygen therapy.

IV. Enclosures
a) Oxygen tent -
It is a canopy over the head and shoulder orover the entire body of the infant.
FiO2 - 40-60%
Oxygen flow - 12 to 15L/min
Provides concurrent aerosol therapy
It is a variable performance device

- Cumbersome
- Limits patient mobility
- Constant leakage
- Risk of explosion
- Difficult to clean.

b) Oxygen hood
It covers only the head of the infant oxygen isdelivered to the hood through either a heatedentrainment nebulizer or a blending system.FiO2 - 21 to 100%
Minimum flow - = 7L/min to prevent oxygenaccumulation.

c) Incubator
Polymethyl Methacrylate enclosure that combinesservo controlled convection heating withsupplemental oxygen. Provides temperaturecontrol
FiO2 - 40 to 50%
Flow rate - 8-15L/min
Advantages :
- Temperature Controlled.
- Humidification possible.
- Multiple access port for nursing.
- Scavenging mechanism inbuilt.
- Infant can be transpoted.

V. Blow Over Oxygen
- Designed for short period only
- Used in children requiring small amount ofoxygen to correct transient respiratorycompromise.
VI. Oxygen Conserving devices
Oxygen therapy on long term basis is costly. Inrecent years several devices with improvedefficacy of oxygen delivery have been introducedto conserve oxygen. Three types of such devicesare available .
They include:
a) Reservoir Cannulae -
These nasal Cannulae store 20ml of oxygenduring exhalation in a reservoir which becomeavailable as a bolus at the beginning of inhalation.Two types of reservoir :
i) Pendant reservoir ( oxymizer pendant)
- Coupled to the nasal prongs and consistsof a collapsing chamber that hangs at the chest.
ii) Moustache configured oxymizer that sitsright on the face
Both reservoirs provide equivalent oxygen savingat a flow rate of 0.5L/min

b) Demand pulse –oxygen delivery devices
- These electronic demand devices delivera pulse of oxygen during early inspiration andnot throughout ventilator cycle. Delivery ofoxygen during exhalation is saved.
It consists of a box shaped unit attached to theoutlet of oxygen source and a solenoid valvewhich open on sensing the decreased pressureduring inhalation. A pulsed volume of 15-35mlof oxygen is delivered each time.
These are also available for use with portablecylinders as well as with piped-in-oxygen systemin hospitals.
c) Transtracheal Catheters
Narrow lumen catheters resemblingangiocatheter. It is inserted directly into trachea.Oxygen is delivered through a tubing attachedto a small fitting at the neck.

VII. Extra Corporeal MembranceOxygenation(ECMO). ECMO pumps and oxygenate a patient's bloodoutside the body allowing the heart and lungs torest. It helps to keep the tissues well oxygenated.Most often ECMO is used in newborn and youngchildren. It can also be used as a last resort foradults whose heart or lungs are failing.In new born ECMO is used to support or replacean infant's underdeveloped or failing lungs byproviding oxygen and removing CO2 wasteproducts, so that the lungs can rest. Indicationsin newborn and young children include -
- Meconium aspiration syndrome
- Persistant pulmonary hypertension
- Congenital diaphragmatic hernia
- Respiratory distress syndrome
- Blood poisoning.

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