Добавил:

Sekretar kiopkiopkiop18@yandex.ru t.me/Prokururor I Вовсе не секретарь, но почту проверяю Опубликованный материал нарушает ваши авторские права? Сообщите нам.

Вуз:

Ростовский Государственный Медицинский Университет

Предмет:

Медицина общая

Файл:

@xirurgi_2025 - 863 - файл

.pdf

Скачиваний:

Добавлен:

29.08.2026

Размер:

10 Мб

Скачать

☆

<<< < Предыдущая 25 26 27 28 29 30 31 32 33 34 35 3637 / 4937 38 39 40 41 42 43 44 45 46 47 48 49 > Следующая >>>

342

https://t.me/med1917

342

CHAPTER40 Military burns

Speciﬁc Causes 1.Explosive Weapons

Physics

• Detonation causes an increase in pressure, which creates a blast wave

or blast wind. The blast wave is high pressure travelling greater than the speed of sound. The blast wind is due to the blast wave displacing the surrounding air

• Burns arise from ashes, due to the primary eect of the explosives, or

ames, due to secondary eect of explosives, eg. igniting clothing

Pathology

• Primary (barotrauma)

• Blast wave aects air– tissue interfaces, eg. ear, lung, gastrointestinal tract. Happens within 10 metres of epicentre and is not protected by body armour

• Secondary (fragmentation)

• Penetrating trauma from surroundings. Occurs up to 1,000 metres from epicentre

• Tertiary (displacement)

• Displacement due to the blast wind causing blunt and penetrating trauma, compartment syndrome, and traumatic amputation.

• Quaternary (miscellaneous, eg. burn)

• Aects 725% people in an explosion

Eect

• Ear. Tympanic membrane rupture. Aects 795% therefore is a sensitive

11,12

marker.

Causes transient sensorineuronal deafness (resolves in

hours/ days)

• Lung. From pneumothoraces to oedema and respiratory failure. Aects

up to 50% of people who die.12 Blast lung syndrome is characterized by triad of dyspnoea, bradycardia, and hypotension. Chest X- ray shows bilateral pulmonary inltrates in a buttery pattern but CT is more sensitive. Arterial air emboli can be seen in the retinal vessels and may cause cerebrovascular accident, myocardial infarction, and intestinal ischaemia

• Gastrointestinal. Ruptured hollow viscera secondary to haemorrhage

and ischaemia

• Ocular. From conjunctival haemorrhage to ruptured globes. Aects 710%

• Musculoskeletal. Associated with traumatic amputations and mortality and therefore requires aggressive intervention. Aects 77%

• Central. From cerebral contusion to intracranial haemorrhage. ‘Shell shock’ encompasses concussive syndrome, post- traumatic stress disorder, and memory dysfunction

https://t.me/med1917

SPECIFIC CAUSES 1.EXPLOSIVE WEAPONS

Management

• General. ATLS

• Ear. >5% rupture10 is referred for tympanoplasty

• Lung. Oxygen. Thoracostomies are performed before anaesthetic or

air transport. During ventilation high pressures are avoided to prevent air embolism and pneumothorax. Hyperbaric oxygen is considered for arterial emboli

• Gastrointestinal. Laparotomy if perforation

• Ocular. Irrigation for 60 minutes if chemical burns and specialist

opinion sought

• Musculoskeletal. Gross deformity is re- aligned and fractures splinted.

Surgical debridement is performed

Outcome

• Extent of injury depends upon amount and composition of material,

delivery method, surrounding environment, and distance between victim and blast

• Explosions cause more polytrauma than any other wounding agent

• Secondary eects of blasts are the leading cause of injury and death in

military attacks

11,12

343

344

https://t.me/med1917

344

CHAPTER40 Military burns

Speciﬁc causes 2.Incendiary weapons

White phosphorous

Pathology

• Thermal and chemical burn via ignition on contact with air

Eect

• Full thickness burn with deeper extension due to high lipid solubility. Systemically causes multi- organ dysfunction

Management

• First aid via removing clothes, irrigating wound, and resuscitation with IV uids

• Remove phosphorous particles. Ultraviolet light (Wood’s lamp) is used to visualize particles. No evidence that copper sulphate aids visualization more and may cause renal failure if systemic absorption

• Excise non- viable tissue

Napalm

Pathology

• Gel mixed with petroleum that sticks to skin

Eect

• Full thickness burns with deeper extension. 10% TBSA burn can cause renal failure. Explosion can cause carbon monoxide (CO) poisoning

Management

• First aid via removing clothes, irrigating wound and resuscitation with IV uids

• Remove napalm from skin

• If CO poisoning give 100% oxygen

• Excise non- viable tissue

Speciﬁc causes 3.Chemical weapons

Sulphur mustard gas

Pathology

• Gas or yellow- brown liquid that smells like mustard. Causes chemical burns via lipophilic action. Breaks down slowly and can damage DNA but is not usually fatal

Eect

• Produces blistering partial thickness burns with slow wound healing

Management

• Move patient to higher ground as it is heavier than air and therefore settles in low- lying areas

• First aid via removing clothes, irrigating wound, and resuscitation with IV uids

https://t.me/med1917

SPECIFIC CAUSES 4.COLD BURNS

Speciﬁc causes 4.Cold burns

Frostbite

Denitions

• Frostnip causes tissue cooling without destruction

• Frostbite causes tissue damage at temperatures below freezing point (70.55°C)

Pathology

• At temperatures below 0°C blood vessels constrict and glomus bodies in the dermis shunt blood away from the extremities

Eect

• Symptoms include pain developing later to numbness

• Examination reveals a cold area, erythematous tissues developing later to black necrosis, blisters containing initially clear developing later to haemorrhagic uid, and oedema

Management

• General management includes prevention (eg. protective clothing), elevation to prevent oedema, and splinting to prevent excessive movement which causes ice crystals. Rewarming is performed passively (eg. blanket) and actively (eg. whirlpool devices), and slowly for nonfreezing injuries but quickly for freezing cold injuries (740°C for 30 minutes twice daily until thawing). Frostbite is not rewarmed until the risk of refreezing is small otherwise more damage occurs

• Medical management includes analgesia, antibiotics, and tetanus toxoid if necrotic tissue. Aloe vera an inhibitor of thromboxane is used for dressings every 6 hours. Thrombolysis is used if major frostbite presents <24 hours post injury and major tissue loss is predicted. Vasodilatory drug infusion, eg. Iloprost is used if major frostbite presents >24 hours post injury

• Surgical debridement is performed early if complicated by infection otherwise delayed until demarcation, which may take up to 72months, or auto- amputation occurs. Clear blisters are debrided but not haemorrhagic ones to prevent desiccation

345

346

https://t.me/med1917

346

CHAPTER40 Military burns

References

1. Jeevaratnam JA, Pandya AN. One year of burns at a role 3 medical treatment facility in Afghanistan. Journal of the Royal Army Medical Corps. 2014;160:22–6.

2. Foster MA, Moledina J, Jeery SLA. Epidemiology of U.K. Military burns. Journal of Burn Care & Research 2011;32:415– 20.

3. Wolf SE, Kauvar DS, Wade CE, Cancio LC, etal. Comparison between civilian burns and combat burns from operation Iraqi Freedom and Operation Enduring Freedom. Annals of Surgery 2006;243:786– 95.

4. Page F, Hamnett N, D’Asta F, Jeery S. Epidemiology of U.K. Military Burns 2008–2013. Journal of Burn Care Research. 2017;38(1):e269–76.

5. Roeder RA, Schulman CI. An overview of war- related thermal injuries. Journal of Craniofacial Surgery 2010;21:971– 5.

6. Atiyeh BS, Hayek SN. Management of war- related burn injuries: lessons learned from recent ongoing conicts providing exceptional care in unusual places. Journal of Craniofacial Surgery 2010;21:1529– 37.

7. Chung KK, Wolf SE, Cancio LC, etal. Resuscitation of severel y burned military casualties:uid begets more uid. Journal of Trauma 2009;67:231– 7.

8. White CE, Renz EM. Advances in surgical care:management of severe burn injury. Critical Care Medicine 2008;36:S318– 24.

9. Gomez R, Murray CK, Hospenthal DR, etal. Causes of mortality by autopsy ndings of combat casualties and civilian patients admitted to a burns unit. Journal of the American College of Surgeons 2009;208:348– 54.

10. Kauvar DS, Wolf SE, Wade CE, Cancio LC, Renz EM, Holcomb JB. Burns sustained in combat explosions in Operations Iraqui and Enduring Freedom (OIF/ OEF explosion bur ns). Burns 2006;32:853– 7.

11. Depalma RG, Burris DG, Champion HR, Hodgson MJ. Blast injuries. New England Journal of Medicine 2005;352:1335– 42.

12. Wolf SJ, Bebarta VS, Bonnett CJ, etal. Blast injuries. Lancet 2009;374:405– 15.

13. Champion HR, Holcomb JB, Young LA. Injuries from explosions:physics, biophysics, pathology, and required research focus. Journal of Trauma 2009;66:1468– 77.

14. Hallam MJ, Cubison T, Dheansa B, Imray C. Managing frostbite. British Medical Journal 2010;341:151– 6.

https://t.me/med1917

Chapter41

347

Sunburn and artiﬁcial tanning

Solar radiation 348 UV radiation 348 Articial tanning 348 Acute harmful eects of UV radiation 349 Erythema 349 Photosensitive reactions 349 Management 350 Further reading 351

348

https://t.me/med1917

348

CHAPTER41 Sunburn and artiﬁcial tanning

Solar radiation

Radiation from the sun is electromagnetic. Most of the solar radiation is blocked by the ozone layer, dust and moisture. The solar spectrum ranges from around 230 to 3,000nm. Visible light and infrared represent the longer wavelengths of the solar radiation spectrum. It is the shorter, ultraviolet (UV) wavelengths that are most harmful.

UV radiation

UV covers the wavelength range 100– 400nm and is divided into three bands.

UVA:400– 315nm

• The longer wavelength penetrates further into the dermis

• Has inuence at a cellular level

• Partly responsible for chronic photo- damage

UVB:315– 280nm

• Erythematogenic

• Stimulates epidermal thickening and melanin production

• Photo- carcinogenic

UVC:280– 100nm

• Blocked by the ozone layer

• Arises from articial sources, eg. germicidal lamps

• Potent photo- carcinogen

Artiﬁcial tanning

• Articial tanning is a $1 billion- a- year industry in the USA alone

• 10% of northern Europeans admitting to regular sun bed use

• This increase in sun bed use is of considerable public health concern,

mainly with regard to skin cancer, but has also been in the public eye more recently as a result of burns sustained due to either ignorance or negligence on the part of the consumer or proprietor

• Sun beds predominantly emit UVA radiation, which is thought to be the

least harmful UV spectrum, with varying levels of the more biologically active UVB (0.2– 3.5%)

• In recent years, sun beds have been manufactured that produce higher

proportions of UVB to mimic the solar spectrum and speed the tanning process

• The incidence of sun bed related burns are increasing

https://t.me/med1917

PHOTOSENSITIVE REACTIONS

Acute harmful eects ofUV radiation

• Pruritus

• Dryness

• Erythema

• Blistering

• Photodrug reactions

• Phototoxic/ photoallergic reactions

Erythema

• Research has reported a biphasic erythema response to UVA:

• Immediate erythema present and maximal at the end of exposure

• Fades partly or completely

• Followed by a later secondary phase of erythema

• The most clinically apparent component of sunburn

• Minimal erythema dose (MED) is the minimum amount of energy

required to produce uniform, clearly demarcated erythema at 24 hours

• Four MED produces painful sunburn, eight MED produces blisters

Photosensitive reactions

• Term applied to abnormal reactions of human skin to UV exposure

• UVA from sun beds can produce photosensitive and phototoxic burns

• Many commonly used medications can cause phototoxic and

photoallergic reactions and are activated in the UVA range

• Psoralens in many common vegetables represent a particularly

dangerous substance

• UV exposure can also exacerbate photosensitive diseases such as

porphyria and systemic lupus erythematosus

349

350

https://t.me/med1917

350

CHAPTER41 Sunburn and artiﬁcial tanning

Management

The mainstay of treatment for sunburn is symptomatic, with regular moisturizing and pain relief. Very few patients require admission. Asuggested treatment algorithm for sunburn is shown in Fig. 41.1.

Public awareness and education must play a part in preventing adverse eects of sun exposure and sun bed use. The increasing incidence of sun bed related burns highlights the need for tighter regulation of the tanning industry.

Sunbed related burn

Small dressings

(e.g. Mepilex Ag,

Mepilex)

District

nurse

OPD dressing

clinic review at

14 days

Discharge with sun care advice and moisturiser

Blistering

Large area or

Pain free able to

go home

OPD dressing

review at 5 days

awkward dressings

Poor pain control

needs admission

Discharge when

pain manageable

and moisturiser

Pain well controlled?

Discharge with sun care advice

Erythema

Admit for analgesia

Discharge when

comfortable with

sun care advice and

NoYes

and elevation

moisturiser

Fig.41.1 Treatment algorithm for sunburn.

https://t.me/med1917