Termal injuries/burns

  Thermal  Injuries/Burns

Ncbi prostalglandin journal

The  British  Burns  Association  has  identified  the  following  as  requiring  referral  to  a  burn  unit:
•  Burns > 10% of total body surface  area  (TBSA)  in  adults  (a  crude  calculation  may  be  made,   assuming  that  the  palm  of  the  patient’s  hand  is  equivalent  to  1%  of  total  body  surface)
•  Burns > 5% TBSA in children
•  Burns of special  areas,  eg  face,  hands,  feet,  genitalia  and  major  joints
•  Full thickness  burns  >  5%  TBSA
•  Electrical  and  chemical  burns
•  Burns associated  with  inhalation  injury
•  Circumferential  burns  of  the  limbs  or  chest
•  Burns in young children  or  the  elderly
•  Burn injuries  in  patients  with  pre-existing  medical  disorders  which  complicate  management,   prolong  recovery  or  effect  mortality
•  Suspected ‘non-accidental  injury’  (NAI).  

Superficial  Burns
a)    Description
Quick  capillary  return.  Red,  slightly  swollen  appearance.  No  blister  formation.  Any  damaged  epithelium may  peel  off  after  5  to  7  days  without  scarring.

b)  Treatment  Aim
•  To relieve pain
•  To protect from infection.

c)  Treatment
•  Immediately place  the  affected  part  under  cold  running  water  (approx  15°C)  for  at  least  20   minutes  (Yuan  et  al  2007). 

This  relieves  pain  and  reduces  the  temperature  of  the  burning process  
•  Remove any clothing  carefully  
•  Apply dressings  as  for  blisters.

Superficial,  Partial  Thickness  Skin  Loss  Burns
a)  Description
Slow  capillary  return.  Epidermis  and  superficial  layers  of  dermis  are  destroyed.  Hair  follicles, sebaceous  and  sweat  glands  are  intact.  This  is  likely  to  be  a  painful  burn  as  the  nerve  endings  have not  been  damaged.   Usually  heals  in  10  to  14  days,  without  scarring.

Deep,  Partial  Thickness  Skin  Loss  Burns a)  Description Slow  capillary  return.  Greater  part  of  the  dermis  is  lost.  Sensation  is  altered.  Patient  may  have  no  pinprick  sensation.

b)  Treatment  Aims  of  Both  Superficial  and  Deep Partial  Thickness  Skin  Loss  Burns
•  To relieve  pain
•  To protect  from  infection
•  To manage exudate. Reproduced  by  permission  of  NHS  Lothian c)  Treatment
•  Immediately place  the  affected  part  under  cold  running  water  (approx  15°C)  for  at  least  10  to  15   minutes  
•  Remove any clothing  carefully  avoiding  any  further  injury.
•  Apply non-adherent  interface  dressing  such  as  Atrauman®.  An  absorbent   secondary  dressing  such  as  polyurethane  foam  film  may  be  used. 

The  primary  dressing  may  be   left  in  place  and  the  secondary  dressing  changed  as  often    as  necessary,  depending  on  choice   of  product  and  exudate  levels. Note:    Silver  sulfadiazine  cream  should  not  be  used  routinely  until  after  specialist  assessment  as  this will  mask  the  wound  bed  and  make  for  difficult  assessment.

Full  Thickness  Skin  Loss  Burns
a)  Description
No  capillary  return. 
No  epithelium  so  burn  can  only  heal  by  contraction,  granulation  and  migration  of epithelium  from  wound  edges.  The  wound  may  look  pale,  charred  and  coagulated  veins  may  be visible.   
No  sensation  is  present  on  testing.  This  will  cause  scarring.

b)  Treatment  Aim
•  To protect from infection
•  To manage exudate.

c)  Initial  Treatment  and  Assessment
•  Immediately place  the  affected  part  under  cold  running  water  (approx  15°C)  for  at  least  10  to  15   minutes.  If  greater  than  3  hours  from  time  of  injury,  cold  water  will  have  no  beneficial  effect.
•  Remove any clothing  carefully  avoiding  any  further  injury.

d)  If  Patient  is  to  be  Transferred  to  Accident  &  Emergency  or  Burns  Unit
•  Cover all burned  areas  primarily  with  cling  film  (which  prevents  infection  and  allows  for  ease  of   assessment)  and  wrap  patient  in  clean  covers  to  prevent  heat  loss  
•  If transfer  journey  is  greater  than  2  to  3  hours,  a  secondary  surgical  absorbent  dressing  of   gauze  and  cotton  tissue  will  be  necessary  to  retain  exudates,  which  may  be  extensive. Note:    Silver  sulfadiazine  cream  should  not  be  used  until  after  specialist  assessment  as  this  will  mask the  wound  bed  and  make  for  difficult  assessment.  

f)  If  Patient  is  not  to  be  transferred
•            Apply primary non-adherent  interface  dressing  such  as  Atrauman®.   
•  Secondary dressings  should  be  highly  absorbent  whilst  maintaining  a  moist  wound  bed  as  thick   eschar  usually  forms.  This  may  be  debrided  surgically  or  by  autolysis.  
•  Treat as for wound type  as  it  progresses  through  wound  healing  stages.
•  Initially,  dressings  may  need  to  be  carried  out  daily  but  this  is  dependent  on  the  amount  of   exudate.
•  Argyll and Bute CHP patient  pathway  is  to  NHS  Greater  Glasgow  &  Clyde.    There  may,   therefore,  be  slight  differences  in  dressings  selection. More  information  is  available  from  the  following  website: http://www.cobis.scot.nhs.uk/

REFERENCE
Yuan  J,  Wu  C,  Holland  AJA,  Harvey  JG,  Martin  HCO,  La  Hei  ER,  Arbuckle  S,  Godfrey  C  (2007)  Assessment  of  cooling  on  an  acute scald  burn  injury  in  a  porcine  model.  J  Burn  Care  Res  28:  514–20.

Cavity wound

  Cavity  Wound

Description
A  wound  which  is  categorised  by  its  depth  and  tissue  involvement.  This  wound  type  may  be  acute  or chronic. Reproduced  by  permission  of  NHS  Lothian

Treatment  Aim
•  To  achieve  management  and  free  drainage of  exudate  
•  To protect  the  surrounding  skin
•  To prevent  infection
•  To remove necrosis  or  slough
•  To promote  granulation  from  the  base  of  the wound.
•  Treatment is dependent  on  the  position  of  the  wound  and  the  amount  of  exudate    (Dealey   2005).

Primary  Dressing  
•  Cavity fillers  e.g.  alginate  rope,  hydrofibre  rope,  

Secondary  Dressing  
•  Polyurethane foam film 19.4  Considerations
•  Rehydration  of  sloughy  wounds  may  increase  the  odour
•  Negative pressure  closure  may  be  indicated,  if  wound  exudate  or  depth  is  significant  (see   Specialist  Products  section)

REFERENCE
Dealey,  C.  (2005)  General  Principles  of  Wound  Management.  In:  The  Care  of  Wounds,d     3rd    edn.  Oxford:  Blackwell  Science.     30 

Necrotic wound

Necrotic  Wound

Description
Brownish/black,  dead  dehydrated  tissue,  leathery  in  texture.  May  be  hard  or  soft. When  an  area  of  tissue  becomes  ischaemic  for  any  length  of  time,  it  will  die.  The  area  may  form  a necrotic  eschar  or  scab. 

When  assessing  these  wounds  it  is  important  to  remember  that  the  wound may  be  more  extensive  than  is  apparent.  The  eschar,  or  slough,  masks  the  true  size  of  the  wound. Unless  necrotic  tissue  is  removed,  the  wound  will  continue  to  increase  in  size.  Intervention  is necessary  for  these  wounds  to  heal  (Dealey  2005). Reproduced  by  permission  of  NHS  Lothian

Treatment Primary  Dressing  
•  Hydrogel/sheet Secondary  Dressing  
•  Hydrocolloid  
•  Polyurethane  Foam  Film

Considerations
•  Debridement •  Wound will  deepen  as  necrosis  is  lifted

Treatment  Aim
•  To remove/debride  dead  tissue  
•  To rehydrate  the  wound.
•  Ischaemic  necrosis-Caution  with  rehydrating  these  wounds: 
Note:    Larval  therapy  is  not  appropriate  for  this  type  of  wound  until  the  necrosis  is  moist

REFERENCE
Dealey,  C.  (2005)  General  Principles  of  Wound  Management.  In:  The  Care  of  Wounds,  3nd  edn.  Oxford:  Blackwell  Science.

Sloughy wound

Sloughy  Wound

Description Viscous,  devitalised  tissue,  predominantly  yellow  in  colour.    It  is  most  often  found  as  patches  on  the wound  surface,  although  it  may  cover  large  areas  of  the  wound.  It  is  made  up  of  dead  cells  which  have accumulated  in  the  exudate.  (Dealey  2005). Reproduced  by  permission  of  NHS  Lothian

Treatment Dry  Slough

Treatment  Aim
•  To remove/debride  slough
•  To remove excess  exudate
•  To promote  autolysis.
•  The aim is to donate fluid  in  order  to  establish  a  moisture  balance  and  promote  autolysis.

Primary  Dressing    
•  Hydrogel/sheet

Secondary  Dressing  
•  Hydrocolloid Wet  Slough
•  The aim is to absorb fluid  in  order  to  establish  a  moisture  balance,  and  promote    autolysis.

Primary  Dressing  
•  Alginate or Fibrous  Hydrocolloid  (depending  on  the  levels  of  exudate)

Secondary  Dressing  
•  Polyurethane  Foam  Film

Considerations
•  larval  therapy  (see  specialist  products  section)
•  sharp  debridement  
•  monitoring  and  management  of  exudate  levels
•  when  using  a  product  that  donates  fluid  ensure  that  the  secondary  dressing  does  not  absorb  the   product  before  the  wound.  i.e.  gel  then  a  foam  product.

REFERENCE
Dealey,  C.  (2005)  General  Principles  of  Wound  Management.  In:  The  Care  of  Wounds,  3rd    edn.  Oxford:  Blackwell  Science. 

Over granulating wound

Over-Granulating Wound

Description 
Granulation tissue which is raised above the level of the surrounding skin. 

Treatment Aim 
• To reduce further development of granulation tissue
• To promote epithelialisation.  

Treatment  Primary Dressing 
• Polyurethane foam film, to provide uniform downwards pressure against the granulation  

Secondary Dressing 
• Only required if primary dressing is non-adherent  

 Considerations 
• Look for signs and symptoms of infection. Hyper-granulation can be encouraged by a bacterial   load.
• Trialling an antimicrobial applied with a secondary dressing that will provide uniform  downward pressure, as tolerated, on the wound may be of assistance.
• Topical steroids may be of use. Discuss with medical staff or nurse specialists in  your area.                                                               

Granulating wound

Granulating  Wound 

Description
Red,  granular  tissue. The  tops  of  the  capillary  loops  cause  the  surface  to  look  granular.  It  should  be  remembered  that  the walls  of  the  capillary  loops  are  very  thin  and  easily  damaged,  which  explains  why  these  wounds  bleed easily  (Dealey  2005). Reproduced  by  permission  of  NHS  Lothian

Treatment  Aim
•  To protect angiogenesis
•  To maintain moisture  balance.

Treatment Primary  Dressing
•  Alginate
•  Thin hydrocolloid
•  Hydrocolloid
•  Fibrous hydrocolloid
•  Polyurethane foam film  (depending  on  the  levels  of  exudate). Secondary  Dressing
•  Only required  if  primary  dressing  is  non-adherent   Considerations
•  Depending on the depth of  the  wound  cavity  packing  may  be  required.
•  If the wound is prone to bleeding,  alginates  can  be  useful  as  they  have  a  haemostatic  property.  

REFERENCE
Dealey,  C.  (2005)  General  Principles  of  Wound  Management.  In:  The  Care  of  Wounds,  3rd    edn.  Oxford:  Blackwell  Science.

Ephithelialising wound

Epithelialising  Wound

Description Pink,  fragile  tissue. As  the  epithelia  at  the  wound  margins  start  to  divide  rapidly,  the  margin  becomes  slightly  raised  and has  a  bluey-pink  colour.  As  the  epithelia  spread  across  the  wound  surface,  the  margin  flattens.  The new  epithelial  tissue  is  a  pinky-white  colour.  In  shallow  wounds  with  a  large  surface  area,  islets  of epithelialisation  may  be  apparent.  The  progress  of  epithelialisation  may  be  seen  as  the  new  cells  are  a different  colour  from  those  of  the  surrounding  tissue  (Dealey  2005). Reproduced  by  permission  of  NHS  Lothian

Treatment Primary  Dressing  
•  Vapour-permeable  adhesive  film
•  Thin hydrocolloid
•  Hydrocolloid

Treatment  Aim
•  To protect  the  fragile  epithelial  cells
•  To maintain  moisture  balance
•  To promote  new tissue  growth
•  To prevent  infection.
•  Polyurethane foam film  (depending  on  the  levels  of  exudate). Secondary  Dressing   •  Only required  if  primary  dressing  is  non-adhesive   Considerations
•  It is essential  that  the  primary  dressing  does  not  adhere  to  the  wound  base  as  this  can  cause       trauma  on  removal.

REFERENCE
Dealey,  C.  (2005)  General  Principles  of  Wound  Management.    In:  The  Care  of  Wounds,  3rd  edn.  Oxford:  Blackwell  Science. 25 

Abration wound

Abrasions wound

Description
These  are  shearing  and  friction  injuries  that  result  in  a  scraping  or  rubbing  away  of  the  epidermis  or dermis.

Treatment
Treatment  Aim
•  To prevent  infection  and  further  tissue  damage  
•  Abrasions  should  be  cleaned  carefully  to  ensure that  there  are  no  foreign  bodies  embedded  in  the wound  (Dealey  2005).
•  Selection of  a suitable  dressing  depends  on  the  extent  and  depth  of  the  injury.
•  Exudate levels  can  vary  and,  depending  on  the  cause  of  injury,  infection  risks  can  be  high.
•  An occlusive dressing,  such  as  a  thin  hydrocolloid,  which  can  be  left  in  place  for  several  days,   and  also  allows  the  patient  to  bathe  and  shower  with  the  dressing  in  situ.  The  effect  of  such  a dressing  is  to  prevent  the  nerve  endings  drying  out.

This  appears  to  be  the  factor  which  reduces the  pain  (Dealey  2005).
•  Dressings where  both  the  patient  and  the  health  professional  can  see  exudate  levels  and   surrounding  skin  condition  can  be  useful.

REFERENCE
Dealey,  C.  (2005)  The  management  of  patients  with  acute  wounds.Oxford:  Blackwell  Science.  

Surgical wound

Surgical  Wound

Description
A  surgical  wound  is  the  result  of  a  planned  procedure,  either  elective  or  emergency,  where  the clinician  creates  the  wound  in  order  to  perform  a  surgical  procedure.  This  wound  type  is  expected  in general  to  follow  a  rapid,  predictable  pathway  towards  healing  with  minimal  scarring  and  loss  of function.  The  wound  may  be  either  incised  and  closed  (this  wound  heals  by  primary  intention)  OR incised  and  laid  open  (this  wound  heals  by  secondary  intention).For  guidance  see  cavity  wounds.

Wound  Healing  by  Primary  Intention Reproduced  by  permission  of  NHS  Lothian Treatment If  a  dressing  is  required: Treatment  Aim
•  To  restore  physical  integrity  and function  without  infection  and  with the  minimum  of  deformity.    
•  Approximation  of  wound  edges immediately  using  sutures,  clips staples  or  adhesives,  so  that  each layer  (muscle,  subcutaneous  fat  and skin) comes  together,  thereby expediting  haemostasis  and  the healing  mechanism.
•  Occlusive  dressings  should  be  used  post  operatively,  which  may  be  removed  within   48  hours  as  the  wound  should  be  totally  sealed,  thus  preventing  the  ingress  of  bacteria   (Dealey  2005).
•  If there  is  strike  through  or  leakage,  dressing  can  be  replaced  or  reinforced.

Wound  Healing  by  Secondary  Intention Treatment  Aim The  wound  is  left  open  to  heal  by  granulation,  contraction  and  epithelialisation,  for  several  reasons:
•  There may be considerable  tissue  loss,  eg  radical  vulvectomy
•  The surgical  incision  is  shallow,  but  has  a  large  surface  area,  eg  donor  sites
•    There may have  been  infection,  eg  a  ruptured  appendix,  or  an  abscess  may  have  been  drained,   and  free  drainage  of  any  pus  is  essential  (Dealey  2005). Treatment
•  Surgical  wounds  should  be  dressed  according  to  the  wound  type.

REFERENCE
Dealey,  C.  (2005  )  General  Principles  of  Wound  Management.  In:  The  Care  of  Wounds,  3rd  edn.    Oxford:  Blackwell  Science.   23 

Pain control in wound

Pain  Control  In  Wound  Management

Most  wounds  cause  a  certain  amount  of  pain  (Casey  1998)  but  pain  management,  a  key  function  of  all health  professionals,  is  often  poorly  managed. 

Sometimes  pain  can  be  severe  and  ongoing,  such  as with  chronic  wounds,  while  at  other  times  it  may  only  occur  with  initial  injury,  or  during  infection  or during  dressing  change.
Patients  may  experience  pain  as  a  result  of:
•  Products or techniques  used  to  cleanse  wounds  
•  Trauma to the tissues  and  surrounding  skin  when  products  are  removed  
•  Skin excoriation  from  exudates  or  wound  drainage   •  Lack of empathy 
•  Failure to record  patient’s  earlier  reports  of  pain  
•  Infection,  which  can  exacerbate  existing  wound  pain
•  Poor techniques when  using  compression  bandaging. Careful  wound  assessment  is  required,  as  selecting  an  inappropriate  dressing  can  result  in considerable  pain  and  discomfort  (Dealey  1999). 
The  correct  dressing  can  ensure  comfort  and  reduce pain,  especially  during  dressing  change. Emotional  responses  can  also  influence  the  perception  of  pain  and  the  distress  of  having  a  wound. The  way  patients  detect  pain  appears  to  be  related  to  the  type  of  damage  causing  it  (Campbell  1995). Clinically,  pain,  like  wound  types,  can  be  classified  as  acute  or  chronic,  but  will  be  related  to:
•  The type of injury  
•  The location of  the  wound
•  Patient perception  and  previous  experience  
•  The healing process  and  approaches  to  wound  management,  e.g.  choice  of  dressing  and   provision  of  analgesia.
Assessment  Of  Pain Pain  should  be  assessed  prior  to  each  dressing  change  and  appropriate  action  taken  to  address  the identified  cause.  Accurate  assessment  depends  on  subjective  reporting  by  the  patient.  Pain  can  be assessed  effectively  during  ongoing  therapy  by  asking  the  patient  to  rate  his/her  pain.  It  is recommended  that  a  simple  visual  analogue  scale  is  used.

The  patient  should  be  asked  if  the  pain  is  worse  at  any  particular  time  or  during  a  particular  activity  so that  analgesic  doses  can 
be  timed  appropriately.  Patients  should  be  closely  observed  throughout  the dressing  procedure  for  reaction  to  treatment.  

Analgesia Whatever  analgesia  is  used  in  wound  care,  its  effectiveness  should  be  evaluated  continuously.  Failure to  achieve  pain  relief  may  contribute  to  the  depression  and  anxiety  associated  with  chronic  pain.   The  type  of  analgesia  to  be  used  depends  upon:
•  The type  of  wound
•  Whether  the  wound  is  acute  or  chronic
•  The level  of  pain  reported  by  the  patient.
•  Patients  individual  circumstances  e.g.  other  medicines,  co-morbidities Effective  doses  of  analgesics  should  be  given. 

In  chronic  pain,  treatment  should  be  given  often  enough and  regularly  to  provide  continuous  pain  relief.  This  is  preferable  to  giving  analgesics  only  when necessary,  ie  allowing  pain  to  recur  before  giving  further  treatment.

Analgesics should also be given in anticipation of pain, giving careful consideration to any activities which exacerbate pain. In the case of acute pain there is little time to titrate the dose against the patient’s response. Analgesics should be chosen according to assessment of the factors mentioned above.  

The use of non-steroidal anti-inflammatory drugs (NSAIDs) eg aspirin, ibuprofen, diclofenac etc., is common in treating minor injuries and in long-term inflammatory conditions. This is due to their action of inhibiting the production of prostaglandins (inflammatory mediators). If wound pain is ongoing it may not be appropriate to use an NSAID due to their side effects.   The WHO analgesic ladder forms the basis of many approaches to the use of analgesic medicines. There are three essential steps on this ladder.

The Who Analgesic Ladder

REFERENCES

Campbell, J. (1995) Making sense  of pain management. Nursing Times 91, 34-35. Casey, G. (1998) The management of pain in wound care. Nursing Standard 13, 49-54. Dealey, C. (2005) The Care of Wounds, 3rd  ed. Oxford: Blackwell Science.  World Health Organization (1996) WHO Guidelines: Cancer Pain Relief, 2nd ed. Geneva, World Health Organization.     

Clean wound prinsip

Wound  Cleansing

As  a  general  rule,  routine  cleansing  of  wounds  to  remove  bacteria  or  to  reduce  infection  is  unlikely  to be  effective  (Miller  and  Gilchrist  1997). Wound  cleansing  may  be  advocated  to  remove  contaminants  in  the  following  instances:
•  To remove visible  debris  after  a  wound  has  occurred  to  aid  assessment
•  To remove excess slough  and  exudate  
•  To remove any remaining  dressing  material
•  Prior to obtaining  a  microbiology  swab Frequent  washing  of  wounds  is  unnecessary  and  undesirable.

Cleansing  Solutions In  the  past  wounds  were  cleansed  with  antibacterial  solutions.  Studies  comparing  the  effectiveness  of antibacterial  solutions  to  tap  water,  normal  sodium  chloride  0.9%  and  distilled  water  have  found  no difference  in  lowering  bacterial  count  and  no  increased  incidents  of  infection  (Dire  &  Welsh 1990;  Rodeheaver  et  al.  1982) 

Antiseptic  solutions  have  been  reported  to  cause  tissue  damage  and hinder  the  healing  process  and  are  unlikely  to  be  effective  (Hellewell  et  al.  1997). One  study  found  the  infection  rate  lowest  in  wounds  cleansed  with  tap  water.  Tap  water  is  more common  as  a  cleansing  agent  in  clinical  settings  (particularly  community).  It  is  cost-efficient,  copious and  accessible  and  is  the  recommended  wound  cleansing  solution  of  choice.  Routine  use  of  sterile sodium  chloride  0.9%  results  in  a  significant  waste  of  resources. Sterile  sodium  chloride  0.9%,  which  is  an  isotonic  solution,  does  not  impede  the  healing  process, cause  allergic  reactions  or  alter  the  bacterial  flora  of  the  skin.  It  should  be  used  in  the  following situations,  where  tap  water  is  not  recommended:
•  On exposed bone or tendon
•  On skin or bypass graft
•  For severely immunosuppressed    patients

Methods  Of  Cleansing Irrigation  is  the  cleansing  mechanism  recommended  for  removal  of  contaminants.  Scrubbing  causes pain  and  local  tissue  oedema,  which  decreases  host  defences.  Vigorous  cleansing  may  however  be necessary,  in  some  instances,  to  remove  grease  and  dirt  from  traumatic  wounds  which,  if  left  in  situ, can  cause  unsightly  tattooing  of  the  skin  (Miller  &  Glover  1999).

Summary •

Does the wound need to be cleansed?  If  not,  don’t  do  it.

•  Always warm the irrigation  fluid  being  used.  Cooling  the  wound  inhibits  cell  mitosis.

•  Never use cotton wool  or  gauze  swabs  to  clean  wounds  as  they  damage  granulating  tissue  and   shed  fibres,  which  increase  the  risk  of  infection.

REFERENCES Dire,  D.J.  &  Welsh,  A.P.  (1990)  A  comparison  of  wound  irrigating  solutions  used  in  the  emergency  department.  Annals  of  Emergency Medicine  19,  704-708. Hellewell,  T.B.,  Major,  D.A.,  Foresman,  P.A.,  Rodeheaver,  G.T.  (1997)  A  cytotoxicity  evaluation  of  antimicrobial  and  non-antimicrobial  wound cleansers.  Wounds  9,  15-20. Miller,  M.  &  Gilchrist,  B.  (1997)  Understanding  Wound  Cleaning  and  Infection.  London:  Macmillan. Miller,  M.  &  Glover,  D.  (1999)  Wound  Management:  theory  and  practice.  London:  Emap  Healthcare  Ltd. Rodeheaver,  G.,  Bellamy,  W.,  Kody,  M.  et  al.  (1982)  Bactericidal  activity  and  toxicity  of  iodine-containing  solutions  in  wounds.  Archives  of Surgery  117,  181-186.

Nutri wound healing

Nutritional Support for  Wound  Healing Healing of wounds,

whether from accidental injury or surgical intervention, involves the activity of an intricate network of blood cells, tissue types, cytokines, and growth factors.

This results in increased cellular activity, which causes an intensified metabolic demand for nutrients.

Nutritional deficiencies can impede wound healing, and several nutritional factors required for wound repair may improve healing time and wound outcome.

Vitamin A is required for epithelial and bone formation, cellular differentiation, and immune function.

Vitamin C is necessary for collagen formation, proper immune function, and as a tissue antioxidant.

Vitamin E is the major lipid-soluble antioxidant in the skin; however, the effect of vitamin E on surgical wounds is inconclusive.

Bromelain Introduction Douglas MacKay, ND, and  Alan L. Miller, ND Wound healing involves a complex series of interactions between different cell types, cytokine mediators, and the extracellular matrix.

The phases of normal wound healing include hemostasis, inflammation, proliferation, and remodeling.

Each phase of wound healing is distinct, although the wound healing process is continuous, with each phase overlapping the next. Because successful wound healing requires adequate blood and nutrients to be supplied to the site of damage, the overall health and nutritional status of the patient influences the outcome of the damaged tissue.

Some wound care experts advocate a holistic approach for wound patients that considreduces edema, bruising, pain, and healing time following trauma and surgical procedures.

Glucosamine appears to be the rate-limiting substrate for hyaluronic acid production in the wound.

Adequate dietary protein is absolutely essential for proper wound healing, and tissue levels of the amino acids arginine and glutamine may influence wound repair and immune function.

The botanical medicines Centella asiatica  and  Aloe vera  have been used for decades, both topically and internally, to enhance wound repair, and scientific studies are now beginning to validate efficacy and explore mechanisms of action for these botanicals.

To  promote wound healing in the shortest time possible, with minimal pain, discomfort, and scarring to the patient, it is important to explore nutritional and botanical influences on wound outcome. (Altern Med Rev  2003;8(4):359-377) ers coexisting physical and psychological factors, including nutritional status and disease states such as diabetes, cancer, and arthritis. Keast and Orsted1 wittily state, “Best practice requires the assessment of the whole patient, not just the hole in the patient.  All possible contributing factors must be explored.”

Wound repair must occur in a physiologic environment conducive to tissue repair and regeneration. However, several clinically significant factors are known to impede wound healing, including hypoxia, infection, tumors, metabolic disorders such as diabetes mellitus, the presence of debris and necrotic tissue, certain medications, and a diet deficient in protein, vitamins, or minerals.

In addition, increased metabolic demands are made by the inflammation and cellular activity in the healing wound, which may require increased protein or amino acids, vitamins, and minerals.

The objective in wound management is to heal the wound in the shortest time possible, with minimal pain, discomfort, and scarring to the patient. 

At the site of wound closure a flexible and fine scar with high tensile strength is desired. Understanding the healing process and nutritional influences on wound outcome is critical to successful management of wound patients.

Researchers who have explored the complex dynamics of tissue repair have identified several nutritional cofactors involved in tissue regeneration, including vitamins A, C, and E, zinc, arginine, glutamine, and glucosamine.

Botanical extracts from  Aloe vera,  Centella asiatica,  and the enzyme bromelain from pineapple have also been shown to improve healing time and wound outcome.

Eclectic therapies, including topical application of honey, sugar, sugar paste, or Calendula succus to open wounds, and comfrey poultices and hydrotherapy to closed wounds are still in use today. 

Although anecdotal reports support the efficacy of these eclectic therapies, scientific evidence is lacking. The Four  Phases of  Wound Healing Tissue injury initiates a response that first clears the wound of devitalized tissue and foreign material, setting the stage for subsequent tissue healing and regeneration. 

The initial vascular response involves a brief and transient period of vasoconstriction and hemostasis.  A  5-10 minute period of intense vasoconstriction is followed by active vasodilation accompanied by an increase in capillary permeability.

Platelets aggregated within a fibrin clot secrete a variety of growth factors and cytokines that set the stage for an orderly series of events leading to tissue repair.

The second phase of wound healing, the inflammatory phase, presents itself as erythema, swelling, and warmth, and is often associated with pain.  The inflammatory response increases vascular permeability, resulting in migration of neutrophils and monocytes into the surrounding tissue. 

The neutrophils engulf debris and microorganisms, providing the first line of defense against infection. Neutrophil migration ceases after the first few days post-injury if the wound is not contaminated.

If this acute inflammatory phase persists, due to wound hypoxia, infection, nutritional deficiencies, medication use, or other factors related to the patient’s immune response, it can interfere with the late inflammatory

phase.3 In the late inflammatory phase, monocytes converted in the tissue to macrophages, which digest and kill bacterial pathogens, scavenge tissue debris and destroy remaining neutrophils. Macrophages begin the transition from wound inflammation to wound repair by secreting a variety of chemotactic and growth factors that stimulate cell migration, proliferation, and formation of the tissue matrix.

The subsequent proliferative phase is dominated by the formation of granulation tissue and epithelialization. Its duration is dependent on the size of the wound. Chemotactic and growth factors released from platelets and macrophages stimulate the migration and activation of wound fibroblasts that produce a variety of substances essential to wound repair, including glycosaminoglycans (mainly hyaluronic acid, chondroitin4-sulfate, dermatan sulfate, and heparan sulfate) and collagen.

These form an amorphous, gel-like connective tissue matrix necessary for cell migration. New capillary growth must accompany the advancing fibroblasts into the wound to provide metabolic needs. Collagen synthesis and cross-linkage is responsible for vascular integrity and strength of new capillary beds. Improper cross-linkage of collagen fibers has been responsible for nonspecific post-operative bleeding in patients with normal coagulation parameters.4 Early in the proliferation phase fibroblast activity is limited to cellular replication and migration. Around the third day after wounding the growing mass of fibroblast cells begin to synthesize and secrete measurable amounts of collagen.

Collagen levels rise continually for approximately three weeks.  The amount of collagen secreted during this period determines the tensile strength of the wound.

a diet deficient in protein, vitamins, or minerals. In addition, increased metabolic demands are made by the inflammation and cellular activity in the healing wound, which may require increased protein or amino acids, vitamins, and minerals.2

The objective in wound management is to heal the wound in the shortest time possible, with minimal pain, discomfort, and scarring to the patient.  At the site of wound closure a flexible and fine scar with high tensile strength is desired.

Understanding the healing process and nutritional influences on wound outcome is critical to successful management of wound patients.

Researchers who have explored the complex dynamics of tissue repair have identified several nutritional cofactors involved in tissue regeneration, including vitamins A, C, and E, zinc, arginine, glutamine, and glucosamine. Botanical extracts from  Aloe vera,  Centella asiatica,  and the enzyme bromelain from pineapple have also been shown to improve healing time and wound outcome. Eclectic therapies, including topical application of honey, sugar, sugar paste, or Calendula succus to open wounds, and comfrey poultices and hydrotherapy to closed wounds are still in use today.  Although anecdotal reports support the efficacy of these eclectic therapies, scientific evidence is lacking. The Four  Phases of  Wound Healing Tissue injury initiates a response that first clears the wound of devitalized tissue and foreign material, setting the stage for subsequent tissue healing and regeneration.  The initial vascular response involves a brief and transient period of vasoconstriction and hemostasis.  A  5-10 minute period of intense vasoconstriction is followed by active vasodilation accompanied by an increase in capillary permeability. Platelets aggregated within a fibrin clot secrete a variety of growth factors and cytokines that set the stage for an orderly series of events leading to tissue repair. The second phase of wound healing, the inflammatory phase, presents itself as erythema, swelling, and warmth, and is often associated with pain.  The inflammatory response increases vascular permeability, resulting in migration of neutrophils and monocytes into the surrounding Page 360                                                           tissue.  The neutrophils engulf debris and microorganisms, providing the first line of defense against infection. Neutrophil migration ceases after the first few days post-injury if the wound is not contaminated. If this acute inflammatory phase persists, due to wound hypoxia, infection, nutritional deficiencies, medication use, or other factors related to the patient’s immune response, it can interfere with the late inflammatory phase.3 In the late inflammatory phase, monocytes converted in the tissue to macrophages, which digest and kill bacterial pathogens, scavenge tissue debris and destroy remaining neutrophils. Macrophages begin the transition from wound inflammation to wound repair by secreting a variety of chemotactic and growth factors that stimulate cell migration, proliferation, and formation of the tissue matrix. The subsequent proliferative phase is dominated by the formation of granulation tissue and epithelialization. Its duration is dependent on the size of the wound. Chemotactic and growth factors released from platelets and macrophages stimulate the migration and activation of wound fibroblasts that produce a variety of substances essential to wound repair, including glycosaminoglycans (mainly hyaluronic acid, chondroitin4-sulfate, dermatan sulfate, and heparan sulfate) and collagen.

2  These form an amorphous, gel-like connective tissue matrix necessary for cell migration. New capillary growth must accompany the advancing fibroblasts into the wound to provide metabolic needs. Collagen synthesis and cross-linkage is responsible for vascular integrity and strength of new capillary beds. Improper cross-linkage of collagen fibers has been responsible for nonspecific post-operative bleeding in patients with normal coagulation parameters.

4 Early in the proliferation phase fibroblast activity is limited to cellular replication and migration. Around the third day after wounding the growing mass of fibroblast cells begin to synthesize and secrete measurable amounts of collagen.

Collagen levels rise continually for approximately three weeks.  The amount of collagen secreted during this period determines the tensile strength of the wound.

The final phase of wound healing is wound remodeling, including a reorganization of new collagen fibers, forming a more organized lattice structure that progressively continues to increase wound tensile strength.  The remodeling process continues up to two years, achieving 4070 percent of the strength of undamaged tissue at four weeks.2 Figure 1 summarizes the phases of wound healing and nutrients that impact the various phases.

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Stroke:  

Gejala dan Penatalaksanaan Ismail Setyopranoto Kepala Unit  Stroke  RSUP Dr Sardjito/ Bagian Ilmu Penyakit Saraf, Fakultas Kedokteran Universitas Gadjah Mada, Yogyakarta, Indonesia 

PENDAHULUAN Stroke  adalah gangguan fungsional otak fokal maupun global akut, lebih dari 24 jam, berasal dari gangguan aliran darah otak dan bukan di- sebabkan oleh gangguan peredaran darah otak sepintas, tumor otak,  stroke  sekunder  karena trauma maupun infeksi (WHO MONICA,  1986). Stroke  dengan defisit neurologik yang terjadi tiba-tiba dapat disebabkan oleh iskemia atau perdarahan otak.  Stroke  iskemik disebabkan oleh oklusi fokal pembuluh darah otak yang menyebabkan turunnya suplai oksigen dan glukosa ke bagian otak yang mengalami oklusi (Hacke, 2003). 

Munculnya tanda dan gejala fokal atau global pada  stroke  disebabkan oleh penurunan aliran darah otak. Oklusi dapat berupa trombus, embolus, atau tromboembolus, menyebabkan hipoksia sampai anoksia pada salah satu daerah percabangan pembuluh darah di otak tersebut.  Stroke  hemoragik dapat berupa perdarahan intraserebral atau perdarahan subrakhnoid (Bruno  et al., 2000). 

 EPIDEMIOLOGI  STROKE Pada 1053 kasus  stroke  di 5 rumah sakit di Yogya- karta angka kematian tercatat sebesar 28.3%; sedangkan pada 780 kasus  stroke  iskemik adalah 20,4%, lebih banyak pada laki-laki.  Mortalitas pasien  stroke  di RSUP Dr Sardjito Yogyakarta men- duduki peringkat ketiga setelah penyakit jantung koroner dan kanker, 51,58% akibat  stroke  hemo- ragik, 47,37% akibat  stroke  iskemik, dan 1,05% akibat perdarahan subaraknoid (Lamsudin, 1998). Penelitian prospektif tahun 1996/1997 men- dapatkan 2.065 pasien  stroke  dari 28 rumah sakit di Indonesia (Misbach, 2000). Survei Departemen Kesehatan RI pada 987.205 subjek dari 258.366 rumah tangga di 33 propinsi mendapatkan bahwa  stroke  merupakan penyebab kematian utama pada usia > 45 tahun (15,4% dari seluruh kematian). Prevalensi stroke  rata-rata adalah 0,8%, tertinggi  1,66% di Nangroe Aceh Darussalam dan  terendah 0,38% di Papua (RISKESDAS, 2007).  Di Unit Stroke RSUP Dr Sardjito, sejak berdirinya pada tahun 2004, terlihat peningkatan jumlah kasus terutama  stroke  iskemik akut  (Tabel 1). (Laporan Tahunan Unit  Stroke, 2009). 

 PATOLOGI   STROKE Infark Stroke infarct  terjadi akibat kurangnya aliran darah ke otak. Aliran darah ke otak normalnya adalah 58 mL/100 gram jaringan otak per menit; jika turun hingga 18 mL/100 gram jaringan otak per menit, aktivitas listrik neuron akan terhenti meskipun struktur sel masih baik, sehingga gejala klinis masih reversibel. Jika aliran darah ke otak turun sampai <10 mL/100 gram jaringan otak per menit, akan terjadi rangkai- an perubahan biokimiawi sel dan membran yang ireversibel membentuk daerah infark. Perdarahan Intraserebral Kira-kira 10%  stroke  disebabkan oleh perdarah- an intraserebral. Hipertensi, khususnya yang tidak terkontrol, merupakan penyebab utama. Tabel 2.  Faktor Risiko  Stroke Bisa dikendalikan Penyebab lain adalah pecahnya aneurisma, malformasi arterivena, angioma kavernosa, alkoholisme, diskrasia darah, terapi antikoa- gulan, dan angiopati amiloid. Perdarahan Subaraknoid Sebagian besar kasus disebabkan oleh pecahnya aneurisma pada percabangan arteri-arteri besar. Penyebab lain adalah malformasi arteri- vena atau tumor. 

FAKTOR RISIKO  STROKE Beban akibat  stroke  mencapai 40 miliar dollar setahun, selain untuk pengobatan dan pera- watan, juga akibat hilangnya pekerjaan serta turunnya kualitas hidup (Currie  et al., 1997). Kerugian ini akan berkurang jika pengendalian faktor risiko dilaksanakan dengan ketat (Cohen, 2000).  (Tabel 2 ). Potensial bisa dikendalikan  Hipertensi  Penyakit  Jantung  Fibrilasi  atrium  Endokarditis  Stenosis  mitralis  Infark  jantung  Merokok Anemia sel sabit Transient Ischemic Attack (TIA)  Diabetes  Melitus  Hiperhomosisteinemia Hipertrofi ventrikel kiri  Stenosis  karotis  asimtomatik. 

Tidak bisa dikendalikan  Umur  Jenis  kelamin  Herediter  Ras  dan  etnis  Gen.

TANDA DAN GEJALA STROKE Serangan  stroke  jenis apa pun akan menimbul- kan defisit neurologis yang bersifat akut (De Freitas  et al., 2009) 

 Tanda dan gejala stroke (De Freitas  et al., 2009)   

Tanda dan Gejala  Hemidefisit  motorik,  Hemidefisit  sensorik,  Penurunan  kesadaran, Kelumpuhan nervus fasialis (VII) dan hipoglosus (XII) yang bersifat sentral, Gangguan fungsi luhur seperti kesulitan ber bahasa  (afasia) dan gangguan fungsi intelektual  (demensia), Buta separuh lapangan pandang (hemianopsia),  Defisit  batang  otak. 

PENATALAKSANAAN  ( PERDOSSI, 2007 ): STADIUM HIPERAKUT Tindakan pada stadium ini dilakukan di Insta- lasi Rawat Darurat dan merupakan tindakan resusitasi serebro-kardio-pulmonal bertujuan agar kerusakan jaringan otak tidak meluas. Pada stadium ini, pasien diberi oksigen 2 L/menit dan cairan kristaloid/koloid; hindari pemberian cairan dekstrosa atau salin dalam H2O. Dilakukan pemeriksaan  CT scan  otak, elektro- kardiografi, foto toraks, darah perifer lengkap dan jumlah trombosit,  protrombin time/INR, APTT, glukosa darah, kimia darah (termasuk elek- trolit); jika hipoksia, dilakukan analisis gas darah.   Tindakan lain di Instalasi Rawat Darurat adalah memberikan dukungan mental kepada pasien serta memberikan penjelasan pada keluarganya agar tetap tenang. 

STADIUM AKUT Pada stadium ini, dilakukan penanganan faktor- faktor etiologik maupun penyulit. Juga dilakukan tindakan terapi fisik, okupasi, wicara dan psikologis serta telaah sosial untuk membantu pemulihan pasien. 

Penjelasan dan edukasi kepada keluarga pasien perlu, menyangkut dampak stroke  terhadap pasien dan keluarga serta tata cara perawatan pasien yang dapat dilakukan  keluarga. 

Stroke  Iskemik Terapi umum: Letakkan kepala pasien pada posisi 30 derajat, kepala dan dada pada satu bidang; ubah posisi tidur setiap 2 jam; mobilisasi dimulai bertahap bila hemodinamik sudah stabil. 

Selanjutnya, bebaskan jalan napas, beri oksi- gen 1-2 liter/menit sampai didapatkan hasil analisis gas darah. Jika perlu, dilakukan intubasi. Demam diatasi dengan kompres dan antipiretik, kemudian dicari penyebabnya; jika kandung kemih penuh, dikosongkan (sebaiknya dengan kateter intermiten). Pemberian nutrisi dengan cairan isotonik, kristaloid atau koloid 1500-2000 mL dan elek- trolit sesuai kebutuhan, hindari cairan mengan- dung glukosa atau salin isotonik. Pemberian nutrisi per oral hanya jika fungsi menelannya baik; jika didapatkan gangguan menelan atau kesadaran menurun, dianjurkan melalui slang nasogastrik. 

Kadar gula darah >150 mg% harus dikoreksi sampai batas gula darah sewaktu 150 mg% dengan insulin  drip  intravena kontinu selama 2-3 hari pertama. Hipoglikemia (kadar gula darah < 60 mg% atau < 80 mg% dengan gejala) di- atasi segera dengan dekstrosa 40% iv sampai kembali normal dan harus dicari penyebabnya. 

Nyeri kepala atau mual dan muntah diatasi dengan  pemberian obat-obatan sesuai gejala. Tekanan darah tidak perlu segera diturunkan, kecuali bila tekanan sistolik  ≥220 mmHg, diastolik  ≥120 mmHg,  Mean Arterial Blood Pressure  (MAP)  ≥  130 mmHg (pada 2 kali pengukuran dengan selang waktu 30 menit), atau didapatkan infark miokard akut, gagal jantung kongestif serta gagal ginjal. Penurunan tekanan darah maksimal adalah 20%, dan obat yang direkomendasikan: natrium nitro- prusid, penyekat reseptor alfa-beta, penyekat ACE, atau antagonis kalsium. Jika terjadi hipotensi, yaitu tekanan sistolik  ≤ 90 mm Hg, diastolik  ≤70 mmHg, diberi NaCl 0,9% 250 mL selama 1 jam, dilanjutkan 500 mL selama  4 jam dan 500 mL selama 8 jam atau sampai hipotensi dapat diatasi. Jika belum ter- koreksi, yaitu tekanan darah sistolik masih < 90 mmHg,  dapat diberi  dopamin  2-20  μg/kg/menit sampai tekanan darah sistolik  ≥  110 mmHg. Jika kejang, diberi diazepam 5-20 mg iv pelan- pelan selama 3 menit, maksimal 100 mg per   hari; 

dilanjutkan pemberian antikonvulsan per oral (fenitoin, karbamazepin). Jika kejang muncul setelah 2 minggu, diberikan antikonvulsan peroral jangka panjang. Jika didapatkan tekanan intrakranial meningkat, diberi manitol bolus intravena 0,25 sampai 1 g/ kgBB per 30 menit, dan jika dicurigai fenomena rebound  atau keadaan umum memburuk, di- lanjutkan 0,25g/kgBB per 30 menit setiap 6 jam selama 3-5 hari. Harus dilakukan pemantauan osmolalitas (<320 mmol); sebagai alter- natif, dapat diberikan larutan hipertonik (NaCl 3%) atau furosemid. 

Terapi khusus: Ditujukan untuk reperfusi dengan pemberian antiplatelet  seperti aspirin dan anti koagulan, atau yang dianjurkan dengan trombolitik rt-PA (recombinant tissue Plasminogen Activator). 

Dapat juga diberi agen neuroproteksi, yaitu sitikolin atau pirasetam (jika didapatkan afasia). Stroke Hemoragik Terapi umum Pasien  stroke  hemoragik harus dirawat di ICU jika volume hematoma >30 mL, perdarahan intraventrikuler dengan hidrosefalus, dan ke- adaan  klinis cenderung memburuk. Tekanan darah harus diturunkan sampai tekanan darah premorbid atau 15-20% bila tekanan sistolik >180 mmHg, diastolik >120 mmHg, MAP >130 mmHg, dan volume hema- toma bertambah. 

Bila terdapat gagal jantung, tekanan darah harus segera diturunkan dengan labetalol iv 10 mg (pemberian dalam 2 menit) sampai 20 mg (pemberian dalam 10 menit) maksimum 300 mg; enalapril iv 0,625-1.25 mg per 6 jam; kaptopril 3 kali 6,25-25 mg per oral. Jika didapatkan tanda tekanan intrakranial meningkat, posisi kepala dinaikkan 30derajat, posisi kepala dan dada di satu bidang, pemberian manitol (lihat penanganan  stroke  iskemik), dan hiperventilasi (pCO2  20-35 mmHg). 

Penatalaksanaan umum sama dengan pada stroke  iskemik, tukak lambung diatasi dengan antagonis H2 parenteral, sukralfat, atau inhi- bitor pompa proton; 

komplikasi saluran napas dicegah dengan fisioterapi dan diobati dengan antibiotik spektrum luas. 

Terapi khusus Neuroprotektor dapat diberikan kecuali yang ber- sifat vasodilator. Tindakan bedah mempertimbangkan usia dan letak perdarahan yaitu pada pasien yang kondisinya kian memburuk dengan perdarahan serebelum berdiameter >3 cm3, hidro- sefalus akut akibat perdarahan intraventrikel atau serebelum, dilakukan VP-shunting, dan perdarah- an lobar >60 mL dengan tanda peningkatan tekanan intrakranial akut dan ancaman herniasi.   

Pada perdarahan subaraknoid, dapat diguna-kan antagonis Kalsium (nimodipin) atau tindakan bedah (ligasi, embolisasi, ekstirpasi, maupun gamma knife) jika penyebabnya adalah aneu- risma atau malformasi arteri-vena (arteriove- nous malformation, AVM). 

STADIUM SUBAKUTTindakan medis dapat berupa terapi kognitif, tingkah laku, menelan, terapi wicara, dan bladder training (termasuk terapi fisik). 

Meng-ingat perjalanan penyakit yang panjang, di- butuhkan penatalaksanaan khusus intensif pasca stroke di rumah sakit dengan tujuan kemandirian pasien, mengerti, memahami dan melaksanakan program preventif primer dan sekunder.  

Terapi fase subakut:- Melanjutkan terapi sesuai kondisi akut sebelumnya,- Penatalaksanaan komplikasi,- Restorasi/rehabilitasi (sesuai kebutuhan pasien), yaitu fisioterapi, terapi wicara, terapi kognitif, dan terapi okupasi, - Prevensi sekunder- Edukasi keluarga dan Discharge Planning

SIMPULANTujuan penatalaksanaan komprehensif pada kasus stroke akut adalah: (1) meminimalkan jumlah sel yang rusak melalui perbaikan jaringan penumbra dan mencegah perdarahan lebih lanjut pada perdarahan intraserebral, (2) men-cegah secara dini komplikasi neurologik mau- pun medik, dan (3) mempercepat perbaikan fungsi neurologis secara keseluruhan. Jika secara keseluruhan dapat berhasil baik, prog- nosis pasien diharapkan akan lebih baik.  Pengenalan tanda dan gejala dini stroke dan upaya rujukan ke rumah sakit harus segera dilakukan karena keberhasilan terapi stroke sangat ditentukan oleh kecepatan tindakan pada stadium akut; makin lama upaya rujukan ke rumah sakit atau makin panjang saat antara serangan dengan pemberian terapi, makin buruk prognosisnya. 

DEFTAR PUSTAKA1. Bruno A, Kaelin DL, Yilmaz EY. The subacute stroke patient: hours 6 to 72 after stroke onset. In 

Cohen SN. 

Management of Ischemic Stroke. McGraw-Hill. 2000. pp. 53-87.2. Cohen SN. The subacute stroke patient: Preventing recurrent stroke. In 

Cohen SN. Management of Ischemic Stroke. Mc Graw Hill. 2000. pp. 89-109.3. Currie CJ, Morgan CL, Gill L, Stott NCH, Peters A. Epidemiology and costs of acute hospital care for cerebrovascular disease in diabetic and non diabetic populations. Stroke 1997;28: 1142-6. 4. De Freitas GR, Christoph DDH, Bogousslavsky J. Topographic classification of ischemic stroke, in Fisher M. (ed). Handbook of Clinical Neurology, Vol. 93 (3rd series). Elsevier BV, 2009.5. Hacke W, Kaste M, Bogousslavsky J, Brainin M, Chamorro A, Lees K et al.. Ischemic Stroke Prophylaxis and Treatment - European Stroke Initiative Recommendations 2003. 6. Lamsudin R. Stroke profile in Yogyakarta: morbidity, mortality, and risk factor of stroke. In: Lamsudin R, Wibowo S, Nuradyo D, Sutarni S. (eds). Recent Management of Stroke. BKM 1998; Suppl XIV: 53-69.     7. Misbach J. Clinical pattern of hospitalized strokes in 28 hospitals in Indonesia. Med J Indonesia 2000; 9: 29-34. 8. PERDOSSI. Pedoman penatalaksanaan stroke. Perhimpunan Dokter Spesialis Saraf Indonesia (PERDOSSI), 2007 9. Riset Kesehatan Dasar (RISKESDAS) Indonesia. Departemen Kesehatan Republik Indonesia. 2007.10. Toole JF. Cerebrovascular Disorder. 4th ed. Raven Press. New York. 1990.11. WHO. MONICA. Manual Version 1: 1. 1986.