- •Preface
- •List of contributers
- •History, epidemiology, prevention and education
- •A history of burn care
- •“Black sheep in surgical wards”
- •Toxaemia, plasmarrhea, or infection?
- •The Guinea Pig Club
- •Burns and sulfa drugs at Pearl Harbor
- •Burn center concept
- •Shock and resuscitation
- •Wound care and infection
- •Burn surgery
- •Inhalation injury and pulmonary care
- •Nutrition and the “Universal Trauma Model”
- •Rehabilitation
- •Conclusions
- •References
- •Epidemiology and prevention of burns throughout the world
- •Introduction
- •Epidemiology
- •The inequitable distribution of burns
- •Cost by age
- •Cost by mechanism
- •Limitations of data
- •Risk factors
- •Socioeconomic factors
- •Race and ethnicity
- •Age-related factors: children
- •Age-related factors: the elderly
- •Regional factors
- •Gender-related factors
- •Intent
- •Comorbidity
- •Agents
- •Non-electric domestic appliances
- •War, mass casualties, and terrorism
- •Interventions
- •Smoke detectors
- •Residential sprinklers
- •Hot water temperature regulation
- •Lamps and stoves
- •Fireworks legislation
- •Fire-safe cigarettes
- •Children’s sleepwear
- •Acid assaults
- •Burn care systems
- •Role of the World Health Organization
- •Conclusions and recommendations
- •Surveillance
- •Smoke alarms
- •Gender inequality
- •Community surveys
- •Acknowledgements
- •References
- •Prevention of burn injuries
- •Introduction
- •Burns prevalence and relevance
- •Burn injury risk factors
- •WHERE?
- •Burn prevention types
- •Burn prevention: The basics to design a plan
- •Flame burns
- •Prevention of scald burns
- •Conclusions
- •References
- •Burns associated with wars and disasters
- •Introduction
- •Wartime burns
- •Epidemiology of burns sustained during combat operations
- •Fluid resuscitation and initial burn care in theater
- •Evacuation of thermally-injured combat casualties
- •Care of host-nation burn patients
- •Disaster-related burns
- •Epidemiology
- •Treatment of disaster-related burns
- •The American Burn Association (ABA) disaster management plan
- •Summary
- •References
- •Education in burns
- •Introduction
- •Surgical education
- •Background
- •Simulation
- •Education in the internet era
- •Rotations as courses
- •Mentorship
- •Peer mentorship
- •Hierarchical mentorship
- •What is a mentor
- •Implementation
- •Interprofessional education
- •What is interprofessional education
- •Approaches to interprofessional education
- •References
- •European practice guidelines for burn care: Minimum level of burn care provision in Europe
- •Foreword
- •Background
- •Introduction
- •Burn injury and burn care in general
- •Conclusion
- •References
- •Pre-hospital and initial management of burns
- •Introduction
- •Modern care
- •Early management
- •At the accident
- •At a local hospital – stabilization prior to transport to the Burn Center
- •Transportation
- •References
- •Medical documentation of burn injuries
- •Introduction
- •Medical documentation of burn injuries
- •Contents of an up-to-date burns registry
- •Shortcomings in existing documentation systems designs
- •Burn depth
- •Burn depth as a dynamic process
- •Non-clinical methods to classify burn depth
- •Burn extent
- •Basic principles of determining the burn extent
- •Methods to determine burn extent
- •Computer aided three-dimensional documentation systems
- •Methods used by BurnCase 3D
- •Creating a comparable international database
- •Results
- •Conclusion
- •Financing and accomplishment
- •References
- •Pathophysiology of burn injury
- •Introduction
- •Local changes
- •Burn depth
- •Burn size
- •Systemic changes
- •Hypovolemia and rapid edema formation
- •Altered cellular membranes and cellular edema
- •Mediators of burn injury
- •Hemodynamic consequences of acute burns
- •Hypermetabolic response to burn injury
- •Glucose metabolism
- •Myocardial dysfunction
- •Effects on the renal system
- •Effects on the gastrointestinal system
- •Effects on the immune system
- •Summary and conclusion
- •References
- •Anesthesia for patients with acute burn injuries
- •Introduction
- •Preoperative evaluation
- •Monitors
- •Pharmacology
- •Postoperative care
- •References
- •Diagnosis and management of inhalation injury
- •Introduction
- •Effects of inhaled gases
- •Carbon monoxide
- •Cyanide toxicity
- •Upper airway injury
- •Lower airway injury
- •Diagnosis
- •Resuscitation after inhalation injury
- •Other treatment issues
- •Prognosis
- •Conclusions
- •References
- •Respiratory management
- •Airway management
- •(a) Endotracheal intubation
- •(b) Elective tracheostomy
- •Chest escharotomy
- •Conventional mechanical ventilation
- •Introduction
- •Pathophysiological principles
- •Low tidal volume and limited plateau pressure approaches
- •Permissive hypercapnia
- •The open-lung approach
- •PEEP
- •Lung recruitment maneuvers
- •Unconventional mechanical ventilation strategies
- •High-frequency percussive ventilation (HFPV)
- •High-frequency oscillatory ventilation
- •Airway pressure release ventilation (APRV)
- •Ventilator associated pneumonia (VAP)
- •(a) Prevention
- •(b) Treatment
- •References
- •Organ responses and organ support
- •Introduction
- •Burn shock and resuscitation
- •Post-burn hypermetabolism
- •Individual organ systems
- •Central nervous system
- •Peripheral nervous system
- •Pulmonary
- •Cardiovascular
- •Renal
- •Gastrointestinal tract
- •Conclusion
- •References
- •Critical care of thermally injured patient
- •Introduction
- •Oxidative stress control strategies
- •Fluid and cardiovascular management beyond 24 hours
- •Other organ function/dysfunction and support
- •The nervous system
- •Respiratory system and inhalation injury
- •Renal failure and renal replacement therapy
- •Gastro-intestinal system
- •Glucose control
- •Endocrine changes
- •Stress response (Fig. 2)
- •Low T3 syndrome
- •Gonadal depression
- •Thermal regulation
- •Metabolic modulation
- •Propranolol
- •Oxandrolone
- •Recombinant human growth hormone
- •Insulin
- •Electrolyte disorders
- •Sodium
- •Chloride
- •Calcium, phosphate and magnesium
- •Calcium
- •Bone demineralization and osteoporosis
- •Micronutrients and antioxidants
- •Thrombosis prophylaxis
- •Conclusion
- •References
- •Treatment of infection in burns
- •Introduction
- •Clinical management strategies
- •Pathophysiology of the burn wound
- •Burn wound infection
- •Cellulitis
- •Impetigo
- •Catheter related infections
- •Urinary tract infection
- •Tracheobronchitis
- •Pneumonia
- •Sepsis in the burn patient
- •The microbiology of burn wound infection
- •Sources of organisms
- •Gram-positive organisms
- •Gram-negative organisms
- •Infection control
- •Pharmacological considerations in the treatment of burn infections
- •Topical antimicrobial treatment
- •Systemic antimicrobial treatment (Table 3)
- •Gram-positive bacterial infections
- •Enterococcal bacterial infections
- •Gram-negative bacterial infections
- •Treatment of yeast and fungal infections
- •The Polyenes (Amphotericin B)
- •Azole antifungals
- •Echinocandin antifungals
- •Nucleoside analog antifungal (Flucytosine)
- •Conclusion
- •References
- •Acute treatment of severely burned pediatric patients
- •Introduction
- •Initial management of the burned child
- •Fluid resuscitation
- •Sepsis
- •Inhalation injury
- •Burn wound excision
- •Burn wound coverage
- •Metabolic response and nutritional support
- •Modulation of the hormonal and endocrine response
- •Recombinant human growth hormone
- •Insulin-like growth factor
- •Oxandrolone
- •Propranolol
- •Glucose control
- •Insulin
- •Metformin
- •Novel therapeutic options
- •Long-term responses
- •Conclusion
- •References
- •Adult burn management
- •Introduction
- •Epidemiology and aetiology
- •Pathophysiology
- •Assessment of the burn wound
- •Depth of burn
- •Size of the burn
- •Initial management of the burn wound
- •First aid
- •Burn blisters
- •Escharotomy
- •General care of the adult burn patient
- •Biological/Semi biological dressings
- •Topical antimicrobials
- •Biological dressings
- •Other dressings
- •Exposure
- •Deep partial thickness wound
- •Total wound excision
- •Serial wound excision and conservative management
- •Full thickness burns
- •Excision and autografting
- •Topical antimicrobials
- •Large full thickness burns
- •Serial excision
- •Mixed depth burn
- •Donor sites
- •Techniques of wound excision
- •Blood loss
- •Antibiotics
- •Anatomical considerations
- •Skin replacement
- •Autograft
- •Allograft
- •Other skin replacements
- •Cultured skin substitutes
- •Skin graft take
- •Rehabilitation and outcome
- •Future care
- •References
- •Burns in older adults
- •Introduction
- •Burn injury epidemiology
- •Pathophysiologic changes and implications for burn therapy
- •Aging
- •Comorbidities
- •Acute management challenges
- •Fluid resuscitation
- •Burn excision
- •Pain and sedation
- •End of life decisions
- •Summary of key points and recommendations
- •References
- •Acute management of facial burns
- •Introduction
- •Anatomy and pathophysiology
- •Management
- •General approach
- •Airway management
- •Facial burn wound management
- •Initial wound care
- •Topical agents
- •Biological dressings
- •Surgical burn wound excision of the face
- •Wound closure
- •Special areas and adjacent of the face
- •Eyelids
- •Nose and ears
- •Lips
- •Scalp
- •The neck
- •Catastrophic injury
- •Post healing rehabilitation and scar management
- •Outcome and reconstruction
- •Summary
- •References
- •Hand burns
- •Introduction
- •Initial evaluation and history
- •Initial wound management
- •Escharotomy and fasciotomy
- •Surgical management: Early excision and grafting
- •Skin substitutes
- •Amputation
- •Hand therapy
- •Secondary reconstruction
- •References
- •Treatment of burns – established and novel technology
- •Introduction
- •Partial thickness burns
- •Biological membranes – amnion and others
- •Xenograft
- •Full thickness burns
- •Dermal analogs
- •Keratinocyte coverage
- •Facial transplantation
- •Tissue engineering and stem cells
- •Gene therapy and growth factors
- •Conclusion
- •References
- •Wound healing
- •History of wound care
- •Types of wounds
- •Mechanisms of wound healing
- •Hemostasis
- •Proliferation
- •Epithelialization
- •Remodeling
- •Fetal wound healing
- •Stem cells
- •Abnormal wound healing
- •Impaired wound healing
- •Hypertrophic scars and keloids
- •Chronic non-healing wounds
- •Conclusions
- •References
- •Pain management after burn trauma
- •Introduction
- •Pathophysiology of pain after burn injuries
- •Nociceptive pain
- •Neuropathic pain
- •Sympathetically Maintained Pain (SMP)
- •Pain rating and documentation
- •Pain management and analgesics
- •Pharmacokinetics in severe burns
- •Form of administration [21]
- •Non-opioids (Table 1)
- •Paracetamol
- •Metamizole
- •Non-steroidal antirheumatics (NSAID)
- •Selective cyclooxygenasis-2-inhibitors
- •Opioids (Table 2)
- •Weak opioids
- •Strong opioids
- •Other analgesics
- •Ketamine (see also intensive care unit and analgosedation)
- •Anticonvulsants (Gabapentin and Pregabalin)
- •Antidepressants with analgesic effects
- •Regional anesthesia
- •Pain management without analgesics
- •Adequate communication
- •Psychological techniques [65]
- •Transcutaneous electrical nerve stimulation (TENS)
- •Particularities of burn pain
- •Wound pain
- •Breakthrough pain
- •Intervention-induced pain
- •Necrosectomy and skin grafting
- •Dressing change of large burn wounds and removal of clamps in skin grafts
- •Dressing change in smaller burn wounds, baths and physical therapy
- •Postoperative pain
- •Mental aspects
- •Intensive care unit
- •Opioid-induced hyperalgesia and opioid tolerance
- •Hypermetabolism
- •Psychic stress factors
- •Risk of infection
- •Monitoring [92]
- •Sedation monitoring
- •Analgesia monitoring (see Fig. 2)
- •Analgosedation (Table 3)
- •Sedation
- •Analgesia
- •References
- •Nutrition support for the burn patient
- •Background
- •Case presentation
- •Patient selection: Timing and route of nutritional support
- •Determining nutritional demands
- •What is an appropriate initial nutrition plan for this patient?
- •Formulations for nutritional support
- •Monitoring nutrition support
- •Optimal monitoring of nutritional status
- •Problems and complications of nutritional support
- •Conclusion
- •References
- •HBO and burns
- •Historical development
- •Contraindications for the use of HBO
- •Conclusion
- •References
- •Nursing management of the burn-injured person
- •Introduction
- •Incidence
- •Prevention
- •Pathophysiology
- •Severity factors
- •Local damage
- •Fluid and electrolyte shifts
- •Cardiovascular, gastrointestinal and renal system manifestations
- •Types of burn injuries
- •Thermal
- •Chemical
- •Electrical
- •Smoke and inhalation injury
- •Clinical manifestations
- •Subjective symptoms
- •Possible complications
- •Clinical management
- •Non-surgical care
- •Surgical care
- •Coordination of care: Burn nursing’s unique role
- •Nursing interventions: Emergent phase
- •Nursing interventions: Acute phase
- •Nursing interventions: Rehabilitative phase
- •Ongoing care
- •Infection prevention and control
- •Rehabilitation medicine
- •Nutrition
- •Pharmacology
- •Conclusion
- •References
- •Outpatient burn care
- •Introduction
- •Epidemiology
- •Accident causes
- •Care structures
- •Indications for inpatient treatment
- •Patient age
- •Total burned body surface area (TBSA)
- •Depth of the burn
- •Pre-existing conditions
- •Accompanying injuries
- •Special injuries
- •Treatment
- •Initial treatment
- •Pain therapy
- •Local treatment
- •Course of treatment
- •Complications
- •Infections
- •Follow-up care
- •References
- •Non-thermal burns
- •Electrical injury
- •Introduction
- •Pathophysiology
- •Initial assessment and acute care
- •Wound care
- •Diagnosis
- •Low voltage injuries
- •Lightning injuries
- •Complications
- •References
- •Symptoms, diagnosis and treatment of chemical burns
- •Chemical burns
- •Decontamination
- •Affection of different organ systems
- •Respiratory tract
- •Gastrointestinal tract
- •Hematological signs
- •Nephrologic symptoms
- •Skin
- •Nitric acid
- •Sulfuric acid
- •Caustic soda
- •Phenol
- •Summary
- •References
- •Necrotizing and exfoliative diseases of the skin
- •Introduction
- •Necrotizing diseases of the skin
- •Cellulitis
- •Staphylococcal scalded skin syndrome
- •Autoimmune blistering diseases
- •Epidermolysis bullosa acquisita
- •Necrotizing fasciitis
- •Purpura fulminans
- •Exfoliative diseases of the skin
- •Stevens-Johnson syndrome
- •Toxic epidermal necrolysis
- •Conclusion
- •References
- •Frostbite
- •Mechanism
- •Risk factors
- •Causes
- •Diagnosis
- •Treatment
- •Rewarming
- •Surgery
- •Sympathectomy
- •Vasodilators
- •Escharotomy and fasciotomy
- •Prognosis
- •Research
- •References
- •Subject index
H. L. Haller et al.
Surgical steps over the time
State at place of accident, first aid and measures
Preceding clinical treatment
Condition on admission
Former illnesses
Additional injuries
Progression of healing and outcome
Complications
Photo documentation
Traceability and verification of authors
Modern burns management requires multi-profes- sional and interdisciplinary co-operation even between far apart specialists. Thus a system is needed, being able to provide relevant information clearly in due time and over large geographical distances. As only health care personnel with different levels of experience, directly involved in primary care of the patient evaluates the status of the burn wounds initially and draws their conclusions from this, it is essential to provide good photographic material for later evaluation. High quality photo documentation is necessary even under ongoing treatment. Very often, dressing changes are carried out by changing staff; details that might be of importance f or further treatment during dressing change can be reviewed on digital pictures, thus avoiding unnecessary dressing changes only for reviewing the wound. Objective information helps to reduce Chinese whispers, causing wrong therapeutic measures.
But this does not compensate the serious shortcomings linked with it. Due to the linguistic variety and the lack of structure, quality and completeness cannot be verified easily or even not at all.
Undefined sources as basics of systems
Other pitfalls are based on implicit, not really given information, assumed by the documenter or interpreter [28]. So evaluation beyond single patients is extremely difficult. Various solutions use given terms without stating their sources and so using not defined terminologies [27].
Creation of data cemeteries
Collins English Dictionary defines documentation as “the act of supplying with or using documents or references” [11]. The aim of any documentation is to make the documented facts available. In most cases, the focus of such documentations is the gathering of data itself instead of making existing data available and so to create multiple “data cemeteries”.
In some existing documentation systems it is not possible to analyze the collected data statistically.
Missing of contemporary features and functions Only very few systems are able to gather data via mobile devices as for example laptops, tablet PCs or smartphones. Another shortcoming of existing systems is that it is not possible to access evidence-
based knowledge [27].
Shortcomings in existing documentation systems designs
Free text documentation
Despite the evidence Törnvall et al. stated that filling out papers in wound documentation has severe shortcomings compared to computer-assisted wound documentation, many institutions use paper forms for this and include them in the patient’s file [68].
Why does this still happen? On the one hand it is common habit to do so, on the other it is tempting to use a full text description and so not being forced to standardize the observations to be documented. Ostensible advantages of free text documentation are flexible terms, dynamic expressions and the possibility of a more effective, as faster recording by dictation.
Concerning the documentation of burn injuries, burn depth and burn size are the most important facts. Therefore the next sections will discuss the facts including pros and cons. The last section will discuss a computer aided three-dimensional documentation system for burns.
Burn depth
A burn is an injury caused by heat. The depth of the burn wound depends on the temperature and on how long the affected area was exposed to the heat. Furthermore, the extent of a burn injury is influenced by the thermal conductivity of the tissue, skin perfusion and existing isolation layers (hair, hornlike structures etc.) [4]. These parameters change dependent on individual circumstances and age of the
118
Medical documentation of burn injuries
patient [74]. Deep burns are caused either by a strong noxa or lack of the ability to sense pain, (e. g. polyneuropathy, deep unconsciousness) or immobilisation of the affected persons, which does not allow them to leave the area where they are exposed to the noxa. Cooling and cooling effects can reduce the effects of thermal trauma. The development of the definite burn depth is a dynamic process which is generally finished after 48 hours [53]. However, it can go on for several weeks. Initial treatment with tangential excision can most probably reduce a more deepening of necrosis [41].
In adults, temperatures up to 44 °C do not cause irreversible damage to the cells as long as the time of exposure is less than 6 hours. The damage to the cells doubles with each degree more between 44 °C and 51 °C. Below 45 °C, contact time must be several hours to cause partial skin damage, between 45 °C and 51 °C several minutes, between 51 °C and 70 °C several seconds and above these temperatures several split seconds [46].
Davies has shown the relation between impact of temperature, subjective discomfort, occurrence of a partial and a third degree burn injury [12]. Evans (as cited in Davies) showed that 8.4J oule/cm2–13.4 J/cm2 cause redness, 13.4 J/cm2–16.0 J/cm2 cause partial skin burn and 16.4 J/cm2–19.7 J/cm2 cause deep burn injuries of the entire skin. Subjective discomfort can be influenced by any pre-existing condition. Polyneuropathy due to various reasons lead to a retarded sensation of the heat by the patient.
Classification of burn depth
There are various nomenclatures and fundamental characteristics to determine burn depth.
In German-speaking countries burn injuries are classified into three degrees [66].
First-degree burns: Redness and superficial damage of the epithelium without cell death.
Second-degree burns are divided into seconddegree superficial burns and second-degree deep burns. A superficial burn (second-degree a) is associated with blisters, a homogenous red surface and strong pain. The epidermis is damaged. Superficial parts of the dermis are damaged and sequestrated. In case the wound bed is less painful, the burn depth is most likely more severe than a second-degree a burn.
Second-degree deep burns are associated with blisters, light surface and less pain than in 2a burns as the pain sensation is reduced. A thrombosis of the intradermal vessel is characterized by a red net-like pattern that does not disappear when touched. The dermis is severely damaged, hair follicles and glands are preserved.
Third degree burns destroy the epidermis and the tissue appears white or dark after cleaning. The wound bed is not painful, however, intact deeper structures maintain their deep sensibility. Epidermis and dermis are destroyed completely.
In the past an additional classification was fourth degree burns. In fourth degree burns chemical damage, charring and lysis was present. More layers, as for example subcutaneous fatty tissue, sometimes muscles, tendons, bones and joints are damaged [66].
In English-speaking countries burns are divided into superficial and deep burns.
1 and 2a degree burns are called superficial partial thickness burns, 2b degree burns are classified into deep partial thickness burn and full thickness burns.
Classification based on healing time
Burn depth can also be classified according to the healing time. Burns healing within 7 days are classified as superficial or first degree burns, burns healing within 14 days are classified as second degree superficial or partial superficial thickness burns, whereas healing within three weeks is classified as deep partial thickness burns and burns that are only granulating after three weeks are classified as full thickness burns1.
Burn depth as a dynamic process
Clinical supervision of the progression of the burn depth is important with regard to the therapeutic regime and thus the prognosis after burn trauma [53]. Generally, the burn depth can progress in any stage of the burn treatment [65]. Pathophysiologic factors as for example vasoconstriction [59], vasodilatation [55], hypoperfusion due to hypovolemia, decreasing cardiac output and edema [34] and thrombosis [52] can cause a deepening necrosis as well as infection
119
H. L. Haller et al.
[63], edema [45], dehydration [45] and circulary necrosis [43]. Furthermore, local pressure can cause necrosis or can deepen it. Continuous phases of ischemia and reperfusion can also be a reason for a late progressing burn depth [30].
Various papers name hypoxia [35], shock [43], sepsis [10], decreased IL-12 and increased TH-2 cells [7] as well as metabolic disorders as for example decreased glucose uptake and decreased lactate release as reasons for a progressing deepening of the burn wound [49, 64, 69].
Burns in older patients, patients suffering from pathologic vascular alteration, diabetes mellitus and immunosuppression are subject to deepen more easily [65].
Non-clinical methods to classify burn depth
Histologic classification of burn depth
The histologic classification of burn depth is generally based on three-zones-model [29]. The zone of coagulation is surrounded by the capillary zone of stasis which itself is surrounded by the zone of hyperemia.
The histologic classification of burn depth is mostly the method of choice. However, its shortcoming is that the denaturation of protein, which is necessary for staining, makes it impossible to take necrotic i. e. denatured protein as parameter for burn depth. Open vessels are detected by hematoxilin- eosin-staining, denatured collagen is detected by Hinshaw-Pearse-staining. The occurrence of thrombosed vessels as a parameter for necrosis is a very sensitive factor; its prediction is timely limited and is subject to various limitations [73]. For Devgan an interpretation of biopsy reports remains subjective regardless of the histologic method [15].
After 48 hours, burn depth is estimated as definite in the initial phase [53].
Thermography
Thermography is based on the negative correlation between surface temperature and burn depth [37]. This method is distorted by the beginning of wound granulation, so best results can only be achieved within the first three days [15].
Two fundamentally different methods are applied. In static thermography, infrared radiation is measured as temperature [57]; in active dynamic thermography temperature is measured after giving a thermal stimulus. A quantitative determination is carried out by the thermal time constant, i. e. temperature change per time unit after giving thermal stimulus. The thermal properties of tissue depend on its proportion of burn necrosis. In animal experiments, exactness, sensitivity and specificity were 100% in the identification of wounds which healed within 3 weeks [58]. However, very even surrounding conditions are necessary to apply this method successfully.
Ultrasound
Keratinocytes are destroyed at 47 °C, collagen at 65 °C [25]. Moserova et al. showed that in pigs differences between normal and scalded skin could be demonstrated [47]. Cantrell proved the difference between normal and denatured collagen by ultrasound [9]. Bauer and Sauer [5] and Brink et al. [8] could show correlations between depth and tissue necrosis measured by ultrasound. According to Heimbach et al. burn depth is often underestimated by this method. Unfortunately, the clinical application of ultrasound has not shown any advantages for the burn surgeon so far [25, 72].
Vital staining
Vital staining is based on the fact that tissue, which is well supplied with blood, stains, and necrosis does not stain. Leape was the first to test methylene blue together with other substances [38]. An intravenous application of methylene blue stains all body parts that are supplied with blood [75]. Methylene blue is degraded within one week to a green and then to an uncolored substance. Thus, surgical measures can be carried out within the first days.
When applying methylene blue as ointment on the body, it is degraded in all areas supplied with blood and not in the areas where necrosis is present. Heimbach et al. was not able to detect the required sharp demarcation for practical use of this method in his clinical examinations. Both procedures might be inhibited by possible allergies [26].
120