Acute skin failure in ICU

2. INTRODUCTION
PATHOPHYSIOLOGY
CAUSES AND CLASSIFICATIONS
CASE DISCUSSION
DIAGNOSIS
MANAGEMENT
CONCLUSION

3. Introduction
 The concept of an ICU in dermatology setting was
first introduced in 1974 by Prof. Rene Touraine.
 Dermatological diseases accounts for 8%–20% of the
patients visiting emergency outpatient department
globally.

4. Acute Skin Failure refers to a state of tissue
hypoperfusion that leads to tissue death.
Although the skin accounts for 10% to 15% of the
total body weight, it requires 25% to 33% of cardiac
output, and thus, is the largest single organ of the
human body.

5. Introduction
 In view of increased immunosuppressed state,
availability of organ transplant, use of multiple drugs,
malignancies, and indiscriminate use of drugs
including homeopathic and ayurvedic, the
possibility of a patient culminating into acute failure of
skin has increased.

7. Long term complications
Susceptible to infection
Immunity
Pulmonary complications
Edema
Nutrition
Fluids and electrolytes
Thermoregulation
Metabolic
Hemodynamic

8. Hemodynamics
 Persistent inflammation leads to;
 Peripheral vasodilatation
 Increased cutaneous blood flow .
 Edema.
 There is increased blood volume and cardiac
output, which may jeopardize an already
compromised cardiovascular system resulting in
high-output cardiac failure.

9. Thermoregulation
 Hypothermia is a very common .
 Fever in the absence of infection mediated by
interleukin-1, produced by damaged keratinocytes .
 Intraepidermal occlusion of the sweat ducts.
 Sudden onset hypothermia in a relatively stabilized
patient, rather than fever, may be a premonitory sign
of septic shock .

10. Metabolic
 Rise (BMR).
 A hyperglycemic state & glycosuria are common in
(50%) & result from associated pancreatitis and
decreased insulin secretion, relative insulin
resistance, stress.
 Altered glucose metabolism enhances caloric loss by
depleting tissue protein as an energy source.
 Shivering as a compensatory mechanism for
hypothermia, is also highly energy consuming

11. Fluids and electrolytes
 Impaired barrier function of the skin resulting in
increased transepidermal water loss (TEWL), &
enhanced percutaneous fluid loss by transpiration
(proportionate to the raised BMR).
 The average daily fluid loss in adult TEN patients with
approximately 50% body surface area (BSA)
involvement is 3-4 liters.

12. Fluids and electrolytes
 Reduction in the intravascular volume and formation
of hyperosmolar urine.
 This is associated with electrolyte imbalance (low Na+
and high K+), and raised serum levels of urea and
creatinine (prerenal uremia).

13. Fluids and electrolytes
 Patients with TEN & autoimmune bullous disorders
have, in addition, extra loss of Na+, K+ and Cl- in the
blister fluid, Hypophosphatemia is a common
complication aggravating insulin resistance, & altering
the neurological status & diaphragmatic function.
 Patients with acute generalized pustular psoriasis
may develop acute hypocalcaemia secondary to
severe hypoalbuminemia .

14.  Destruction of stratum corneum, the layer mainly
responsible for the barrier function of the skin, cause
up to 40 times increase in fluid loss than the normal
rate of 1 ml/cm2/hour, 50% (BSA) involvement leads
to daily fluid loss of up to 4-5 liters.
Fluids and electrolytes

16. Nutrition
The main causes of hypoproteinemia are
 Continuous loss through shed scales.
 Increased BMR.
 Decreased hepatic synthesis.
 Dermatogenic enteropathy leading to protein loss.
 Dilution due to hypervolemia .

17. Nutrition
 The normal material exfoliated from the skin amounts to
500-1000 mg/day.
 It is increased several folds (9 g/m2 BSA/day) in different
disease states precipitating ASF.
 Diffuse scaling leads to protein loss of approximately 20-30
g/m2 BSA/day.
 In presence of exudative skin lesions, the combined protein
loss through oozing from the skin surface & urine may
amount to 150-200 g/day.

18. Nutrition
 Loss of proteins (40 gm/L), Na (120-150 mmol/L), Cl
(10-90 mmol/L) and K (5-10 mmol/L) in the bullous
fluid leads to decrease in intravascular volume.
 The resultant decrease in urinary output and
increased blood nitrogen can lead to renal failure
unless treated energetically.

19. Nutrition
 The cumulative effect of these factors is a -Ve nitrogen
balance, increased urinary nitrogen &
hypoalbuminemia.
 Muscle wasting.
 In addition to the loss through the shed skin, there is
impaired absorption of iron and vitamin B12 &
folate deficiency, contributing to anemia.

20. Edema
Peripheral edema
1. Increased capillary leakage
2. Hypoalbuminemia
3. Associated cardiac failure
4. Inflammation resulting from the primary skin disease
 VPF & VEGF are cytokines liberated by keratinocytes
which induce dermal capillary proliferation and
enhance micro vascular permeability.

21. Pulmonary Complications
 Severe pulmonary edema (2ry to capillary leak
syndrome) & (ARDS) are complications of
erythroderma.
 Over correction of hypovolemia frequently gives
rise to overt pulmonary edema (30%).

22. Immunity
 Lymphopenia , Neutropenia & Thrombocytopenia
are well-known complications of TEN.
 Impaired chemotaxis & phagocytosis of
granulocytes and low serum gamma globulin levels are
common.
 CD4+ T- lymphocytopenia may be associated even in
the absence of HIV infection.

23. Susceptible for infections
 Damaged skin and its exudates support growth of a
wide spectrum of endogenous & exogenous
organisms leading to systemic infection, severe sepsis
and death.

24. Long Term Complications
 Eye : Ectropion, corneal scarring
 DVT , stress ulcers
 Mucosal involvements:
Esophagus: Stricture, Dysphagia
Urethra: Stricture, Synechiae
Vagina: Stricture, Synechiae
Skin: Pigmentry changes
Hair: Scaring alopecia
Nails: Dystrophy

26. Common dermatoses leading to
ASF
 Clinical spectrum of Erythema multiform ranges
from mild (EM minor) to severe (SJS , complex and
TEN).
 Severe drug reactions.
 Bullous diseases.
 Burn.

27. Erythema multiform
 Acute, self-limiting, mucocutaneous reaction pattern
to many viral, bacterial, protozoa & fungal
infections, tumors, drugs, autoimmune states and
miscellaneous conditions.
 HSV infection is the most frequent cause followed by
mycoplasma pneumoniae.

28. Erythema multiform
 Consists of symmetrically distributed polymorphic
rash classically with iris or target lesions seen on
hands with a central vesicle, or erythema surrounded
by a pale and then a red ring.
 Clinical spectrum of Erythema multiform ranges
from mild (EM minor) to severe (SJS , complex
&TEN).

41.  Morbilliform rash with fever and internal organ
involvement
 “Toxic erythema”
 Mortality - about 10%
 Later onset (2-6 weeks) after new drug commenced
 Fever, lymphadenopathy
 Eosinophilia
 Hepatic / renal failure
 Treatment: withdrawal of offending drug(s) and
supportive care

47.  Immunobullous diseases like pemphigus, pemphigoid,
etc. and hereditary mechanobullous disorders like
epidermolysis bullosa can be disabling and even life-
threatening in some cases.

48.  Pemphigus vulgaris: There are three main types of
pemphigus- P foliaceous, (the blister is in the
superficial granular layers), P vulgaris, (the blisters
form just above the basal layer) & paraneoplastic
pemphigus that occurs in association with malignancy.

49.  Though flaccid blisters are the primary lesions of
pemphigus, erosions are common and usually painful.
 Nikolsky’s sign is positive.

50.  Bullous pemphigoid: This subepidermal blistering
skin disease of the elderly is characterized by large,
tense bullae arising on normal or erythematous skin..

54.  A 74-year-old male patient visited Dongguk University
Gyeongju Hospital with high fever and a drowsy mental
state.
• He was admitted to the intensive care unit (ICU) because of
septic shock due to bacterial pneumonia.
• His MAP dropped to 50–60 mmHg. Initial blood
examination revealed the following: leukocytes, 38,740/μL;
myoglobin, 7,896 ng/mL; creatine kinase >3,000/μL.
• The amount of urine was less than 300 mL/day.
Hemodynamic instability occurred, and was attributed
to acute respiratory failure and acute renal failure.
After 2 weeks of treatment in the ICU, he began to regain
health gradually, and his vital signs stabilized.

55.  In the ICU, to prevent PU, position changes were
performed every 2 hours, using an air mattress.
 Pressure on bony prominences was dispersed by using
a donut-shaped pouch.
 Three days later, despite efforts to prevent PU,
multiple skin ulcers had developed that were not
present at admission.
 The lesions developed simultaneously and
progressed rapidly. Of particular note, the lesion on
the left buttock was not round, but was pear-
shaped, unlike common PU.

56.  Many authors contribute to confusion by
interchangeably using terms that refer to unavoidable
PU-like lesions, such as ASF, unavoidable PU, and
Kennedy terminal ulcer.
 Because of the absence of clear diagnostic criteria,
these terms are often used inappropriately.

57.  Skin failure is defined as an event that causes the skin
and underlying tissue to die due to hypoperfusion
concurrent with severe dysfunction of another
organ system.

58.  The National Pressure Ulcer Advisory Panel defined
unavoidable PU as an ulcer that forms because of an
individual’s clinical conditions & risk factors,
despite the proper application of standard preventative
measures.

59.  A Kennedy terminal ulcer is defined as unavoidable
skin breakdown or skin failure associated with the
dying process.

64. Why ASF not PU ?
1. The multiple skin ulcers were caused by ischemia
secondary to poor perfusion related to septic shock
with multiorgan failure.
2. Multiple skin ulcers occurred despite the
implementation of proper preventative measures.
3. The shapes and locations of the ulcers did not
correspond with those of typical PU.
4. Multiple skin ulcers occurred simultaneously and
rapidly.

66. Diagnosis
 The diagnosis is primarily based on the appearance of
the skin lesions and their typical symmetrical
distribution, especially if known risk factors are
present.

67. Rule of Nines

68. SCORTEN score

71. The following investigations can be done
in all patients
 Complete blood count .
 Serum electrolytes .
 Complete urine examination (hematuria & proteinuria are indicative of
renal involvement) .
 Blood sugars.
 Liver function tests (SGOT , SGPT are slightly elevated in half of the
patients ; or due it frank hepatitis caused by drugs, sepsis or shock) .
 Renal function tests .
 Chest x ray .
 HIV .
 Skin Biopsy ( to confirm the diagnosis).

72. Wound Care Team
Plastic Surgery
Intensivist
Dermatologist
Immunologist & Rheumatology

73.  Promptly discontinue any and all possible
offending drugs .
 Admit the patient in an ICU or burns ward.
 Assess the condition of the patient to determine the
prognosis based on the SCORTEN score.

74. Fluid & electrolyte imbalance
• The fluid requirement is calculated based on the
parklands formula & 3/4ths of this total amount is
given to a pt with TEN
(Parkland’ formula = 4 ml/kg body wt × % BSA).

75. Fluid & electrolyte imbalance
 Isotonic saline 0.7ml/kg/% of BSA affected and
human albumin 1ml/kg/% BSA.
 Potassium phosphate is added to I/V fluids to
prevent insulin resistance. About 1500ml of
nasogastric feed can be given in addition on first
day.

76. Nutritional support
 Patient should be allowed to eat a soft diet.
 Then NGT feeding or parenteral feeding can be
given Early and continuous feeding decreases the risk
of stress ulcers, reduces bacterial dislocation,
enterogenic infection.
 Golden guidance Indirect calorimetry.

77. Nutritional support
 Aggressive nutritional support to compensate the
hypercatabolic state & to promote tissue healing.
 Energy requirement in adults is 1500- 2000 Kcal in
first 24 hrs; with an increment of 500 Kcal daily up
to 3500-4000 Kcal/day.
 Protein intake of 2-3 gms/kg/day (3-4 gms/kg in
children) should help in faster healing.

79. Temperature control
 Nursing in a room at temperature of 30-32°C, in an
air-fluidized bed is helpful.

80. Wound care
 Detached or detachable epidermis should be left
in position as a biological dressing & only the
denuded skin be covered with a dressing.
 Petrolatum impregnated gauzes can be used.

82. Wound care
 Topical antiseptics like silver sulphadiazine
(contraindicated in patients sensitive to sulpha drugs)
should be applied after proper bath/soaks with
potassium permanganate solution.
 Peripheral line is more recommendable than
central, which has a higher chance of infection, but
good peripheral venous access is difficult to find.

83. Wound care
 All lines should be checked for signs of infection daily
and changed two times a week with tips of lines and
catheters sent for culture.
 Care of mucous membranes like eyes, nose, mouth,
genitals, etc., is essential to prevent morbidity and
infections.

84. Ophthalmic care
 2 hourly instillation of eye drops ( saline or
antibiotic drops ) Apply ointments at night.
 Developing synechiae are disrupted by a blunt
instrument.
 Systemic Abx. & Anti-fungal if suspected
endophthalmitis.

86. CORTICOSTEROIDS
 Role of corticosteroids is controversial Systemic
corticosteroids may delay wound healing, increase
the risk of infection, mask early signs of sepsis, and
may precipitate gastrointestinal bleeding .
 But if the involved area is more than 20% of BSA , then
the advantages of treatment outweighs its drawbacks.

87. CORTICOSTEROIDS
 Give oral prednisolone (1-2 mg/kg/day) or parenteral
steroids ( dexamethasone 8-16 mg daily or
hydrocortisone) can be started within the first 72
hours in a patient with limited skin surface
involvement to prevent wide spread diffusion, and
continue for 3-5 days followed by rapid tapering.

88. CYCLOSPORINE
 It acts by inhibiting the activated T lymphocytes,
macrophages & also interferes with the metabolism
of TNF-α and possesses anti apoptotic properties.
 Cyclosporine interrupts the disease progression &
decreases the time taken for complete
reepithelization.

89. CYCLOSPORINE
 Dose is 3-5 mg/kg/day oral or IV up to 2 weeks
followed by weaning over another 2 weeks • Side
effects are hypertension, renal toxicity ( but these
effects are not seen with short duration of treatment).
 Watch out septic complications and severe
leucopenia.

91. INTRAVENOUS
IMMUNOGLOBULINS
 Can be considered if pt is seen within 48-72 hrs. of
bulla onset & in cases with active progressing lesions
even after 72 hrs.
 Total dose is 2 gm/kg , which is given as 0.4
g/kg/day for 5 consecutive days.

92. INTRAVENOUS
IMMUNOGLOBULINS
 Adverse effects are risk of thromboembolism,
hemolysis, vasomotor symptoms & anaphylactic
reactions But the major limiting factor is its high cost.

94. DEXAMETHASONE-
CYCLOPHOSPHAMIDE PULSE
THERAPY
 Involves IV administration of 100 mg of
dexamethasone + 500 mg of cyclophosphamide in 500
ml of 5% dextrose over 1-2 hours on day 1.
 Followed by daily administration of 100 mg of
dexamethasone for the next 2 days.
 These pulses are repeated every 4 weeks.
 Major advantages seen with this therapy are quick
healing of lesions, absence of side effects of
corticosteroids.

96. TNF Alpha Inhibitors
 TNF alpha inhibitors from recent studies are
showing possible mortality benefit, with one such
study form Italy showing improvement in 10/10.
 Patients treated with a single dose of etanercept (50
mg) without significant side effects .

98. Other Lines:
 Tetracycline (2gr/day).
 Nicotinamide ( 1.5gr/day).
 Dapsone (100-300 mg /day).
 Rituximab (375 mg/m2 IV once weekly for 4
consecutive weeks).
 Plasmapheresis.

99. Conclusion
 Sudden severe alterations in the anatomy and
physiology of skin consequent to generalized
dermatoses can lead to disabling complications
eventuating in the potentially fatal syndrome of
acute skin failure.
 Understanding the etiopathogenesis of various
systemic complications of acute skin failure and their
prompt management in ICU on lines similar to that
of burns can salvage many lives.