Lacerations in the ER Part 1: Before you stitch!

Here are my notes from the 'Advanced wound care' lecture, the last lecture before graduation. After just an hour with this prof I felt like I could handle any laceration that comes into the ER. Hopefully after this post you will feel a similar confidence:

History is important!
Before touching the wound, you should know exactly how it happened, when it happened and what instrument/surface cause the laceration. Its important because wounds heal differently and are devitalised in many different ways depending on these factors.

Location is relevant, the face heals better than the hands. Some areas are more mobile and better perfused.

Patient factors;
Patient factors will affect healing and can be important clues for risk of infection (diabetes), healing time etc.
Steroids slow healing, HIV doesnt affect wound healing, Keloids are common in afro-americans.

Find out the patient's Tetanus Status,  you have probably heard about tetanus prone wounds, this is a myth. You can get tetanus from a corneal abrasion. Make you sure you find out about the primary series of vaccinations! no good giving a booster if someone hasn't had their primary series! this is a common situation with immigrants in our ER. Many people forget to ask! CDC advice

The key to good wound practice is IRRIGATION. rememeber: "the solution to pollution is dilution" Water is the best irrigant, you can use plain old tap water, its the volume that matters, taking the patient over to the tap you can supply much more water than a simple syringe from a saline bag. You will never completely eliminate the bacteria, it just needs to have a lower enough concentration so that colonies don't form (sample principle as the lab). Consider the environment, kid falls and hits head on table legvs kid who falls and hits head on road kerb. You need volume and pressure

Sensation:
The gold standard to test sensation is a 2 point discrimination (5mm apart for the hands), make sure there eyes are closed of course. A plastic surgeon can repair most nerves proximal to the DIP joint of the fingers, you will need them to fix any nerve injuries. From a malpractice point of view you need to perform the gold standard.

You can investigate tendon injuries in a variety of ways, a good way to test is to ask the patient to assume the position of  function, you will spot any flexor injuries easily.
Position of function: arms raised to shoulder height, with hands pointing up and open chest position. imagine a policeman says "hands up!"
Flexor injuries you should call the surgeon. There is a small no mans land, the deep palmar lacerations. If the palm hurts when they move their hand then they have probably knicked the palmar sheath. With little pain you can probably leave this but a surgical referral is probably best.
Many extensor tendon injuries can be splinted and will heal well.

Remove foreign bodies. 90% of glass can be seen on X-ray

Use anaesthetic, local anaesthesia or nerve block. nerve blocks are very useful and with ultrasound very easy to perform (with practice). Use Lidocaine (short acting) or Bupivicaine (medium acting 8hours half life). Some areas are tender, for example the sole of the foot, do a nerve block!
Allergic reactions to lidocaine itself are impossible! (only to the preservatives used within, which are rare now). You can be almost 100% sure  there will be no allergic reaction if you use single use vials or cardiac lidocaine.
There has never ever been a documented case of allergci reaction to cardiac lidocaine.
Most lidocaine reactions are just a vasovagal reaction to the needle ha.
When dealing with the face or kids, topical agents are great eg. Tetracaine. You can wack it on in triage.

Explore all Wounds!

Anaesthesia, Betadine on the neighbouring skin surface (not inside the wound). you are ready to suture!

SUMMARY:

• History of injury
• Location considerations
• Pateint factors
• Tetanus status
• Good neurovascular and functional exam
• Irrigation
• Anaesthesia

Get ready to stitch this guy up

Burns

Over 175000 patients visit the emergency department every year with a burns injury in the UK. Burns can be life threatening in the acute phase and severely affect quality of life in the chronic phase with scarring and sometimes even loss of limbs and body parts. Care in the first hours can have a massive impact on the long term outcome, so here is the facts on burns! 

FIRST AID:

If you approach a burns patient outside of hospital adopt the SAFE approach first always.
SAFE: Shout for help, Assess scene (is it safe?), ensure its Free from danger before you approach, Evaluate the casualty (ABCDE)). Pay particular attention to the A for Airway in your primary and secondary surveys and look for signs of inhalation injury (listed below).

After you have done a general assessment of the patient with ABCD, remove any clothing and jewellery around the injury unless they are stuck to the wound, then leave it. 

Manage the burn with the 3 C's:

COOL CALL COVER

Cool the burn with normal running tap water for at least 20 minutes, the water should be around 15 degrees. Cooling is beneficial up to three hours after the burn. The rule is to cool the burn but warm the patient! so make sure the rest of the patient is well covered up, you must prevent hypothermia at all costs. Don't use ice. 

Call an ambulance. 

Cover the injury, use loose clingfilm, on the face you should use wet gauze instead. 

EXAMINATION AND HISTORY:

The severity of a burn is judged by the percentage total body surface affected (%TBSA) and the depth of the burn.

3 methods for Judging %TBSA: 
- Wallaces rule of nines (adults, picture below)
- Lund and Bowder chart (accounts for age differences)
- Number of hands (Area of palmar surface of hand is equal to1%)
Include all burnt areas in the surface area but NOT very superficial burns, with no blistering and only red and dry.

Judging depth of burn, four levels of depth:
(-Superficial (dry, red and painful, normal capillary refill)
-Superficial dermal (erythematous, small blistering, moist, painful, brisk capillary refill)
-Mid-dermal (dark pink, blistered, sluggish capillary refill, dull sensation)
-Deep-dermal (blotchy red, may be blisters still, no refill, no sensation)
-Full thickness (white or black, eschar often present, no refill and insensate)

This system has largely superceded the degrees system but is roughly the same:
superficial dermal=first degree burn
mid-dermal and deep dermal= second degree burn
full thickness= third degree burn
note that deep dermal and full thickness burns will not heal!

You should pay pay aprticular attention to signs of impending airway obstruction; hoarseness, stridor, snoring and smoke induced inhalation injury which can result in airway oedema and obstruction. So look for signs of burns to mouth, nose, face, singed nasal hairrs, carbonacous sputum. 

If any of the burns are circumferential in nature, they could act as a tourniquet with scarring and tissue swelling underneath. This could lead to limb ischemia or even respiratory compromise if the chest wall is involved. You need to look out for this! To preserve the limb the patient may need an 'echarotomy' a surgical incision of the burnt tissue to allow the tissue to expand. 

FLUIDS:

Loss of water from the burnt area and generalised oedema caused by systemic inflammation can cause a life threatening hypovolemia and organ failure.
Start fluids with all burns greater than 15% TBSA using m-Parkland formula below
and aim for a urine output of 0.5ml per kg body weight.
Remember inhalation burns also lead to fluid losses! (you cannot see the extent of internal burns).

The Modified Parkland Formula:
-give 3-4ml Hartmanns solution per kg body weight per %TBSA over 24hours (half given over first 8hours, over half given over next 16hours).

Dilutional hyponatremia is common and so is hyperkalemia with extensive muscle damage. Electrocution burns can cause rhadbomyolysis and myoglobinuria. You may need to increase the fluid resuscitation to prevent acute tubular necrosis from kidney myogobin overload.

MANAGEMENT and pearls:

Inhalation injury management:
-establish patent airway early and consider intubation early. oxygenate and ventilate. Get arterial blood gases and CO levels.

Get tetanus status

Gastroparesis is common and you should consider inserting a NGT.

Patients are often in pain and emotional distress so give IV analgesia early. Consider opioids as first line (titrated to effect).

Avoid antiseptics and dress wounds with non-adherent dressings and gauze, applie covering bandge very loosely. In a first aid setting clingfilm works very well.
-Paraffin gauze and silver sulfadiazine cream, covered with gauze and bandage.

Consider non-accidental injury and abuse, (does the pattern of injury fit the story).

Antibiotics not indicated in early care

Children: start fluids with 10% TBSA burns and aim for urine output of 1ml per kg body wt.

When to refer to a burns specialist/burns centre:

• Any chemical or electrical burn
• Any burn to face, perineum/genitalia, hands and feet
• TBSA greater than 25% second degree burn
• All full thickness burns

Main complications of full thickness/third degree burns:

• Infections, sepsis
• Tetanus
• Hypothermia
• Hypovolemia

Chemical burn management:

-Brush off any powder first, flush the area with copious amounts of water for 20-30minutes. Note duration of exposure and whether chemical is acid or base. 

Surgical management:

(generally by  a plastic surgeon or burns specialist)

Dressing, Escharotomy, Escharectomy, Flaps, Graft

-late escharectomy has better aesthetic outcomes but early escharotomy may be necessary for circulation or ventilation problems. 

Sources:

-Emergency medicine secrets 6th edition Dr Vincent Markovchick 2016

-Student BMJ January 2016 volume 24

-Lecture notes Prof Klinger Humanitas University 2016 and seminar 2015

Forensic medicine: Gun Shot Wounds

Depending on where you are working, gun shot wounds (GSWs) may be a rarity or so common that almost everyday you will see a patient with a GSW in the emergency room. GSWs generally have a bad prognosis with a high incidence of gangrene and anaerobic infection. On top of that there is likely to be a criminal investigation regarding the shooting, so knowledge of how to describe a lesion and preserve evidence is incredibly important. 

When talking about GSWs you first need to consider the construction of the bullet and the mechanics of gunfire. Projectiles are most often made of lead and may be jacketed or not, the jacket is often made of an alloy like brass (copper and zinc alloy). Here in Italy, unjacketed projectiles are illegal.

The bullet contains the projectile, jacket and a small amount of gunpowder which produces the explosion behind which propels the projectile.  The gunpowder usually contains the following chemicals; Barium, Antimony and Lead. These chemicals are what forensics pathologists look for when they look for evidence, they can sometimes even type the gun with knowledge of the chemical ratio.

On pressing the trigger there is a small explosion and most of the gunpowder is burnt to produce gas, however some powder will not burn and be fired along with the projectile.

So when the bullet exits the muzzle of the gun, gas and small fragments of unburnt powder also exits the gun like a kind of small pepper spray, there is also residue and grease from the barrel that is fired along with everything else.

A shotgun bullet is slightly different in that the projectile is actually a collection on small pellets (the shot) as the pellets leave the barrel of the gun they spread out so a GSW from a close range shotgun shot (it forms a large hole) is different to a long range shotgun shot (many small holes).

Bullets may penetrate the body and may exit or stop within the body. They can ricochet off bone and some are actually made to bounce more in the body cavities (nasty). The bullet entry hole is usually much bigger than the actual bullet because as the bullet travels through the air it spins and oscillates (again some are designed to do this more, for more damage). It can sometimes be very difficult to tell the difference between the entrance and exit wound because of this. Bullets may even break and leave multiple exit wounds from a single a entry point or multiple entries. Usually an entrance wound is a round discontinuation with no loss of tissue. The residues from the gun will be on the skin surface around the entrance wound. Its important to use tape or a stub to collect the residue from the skin surface. In fact you should keep anything used to clean the wound and the victims clothes as well as they will contain very important residue.

There are four things you can see with a GSW and it depends on the distance of the victim from the gun.

•        Entry/exit wound

•        Tattooing

•        Smoke stains

•        Burns.

At long distance there will be only the entry and exit wounds from the bullet. As the victim is closer to the attacker tattooing can be seen caused by small pieces of unburnt gunpowder that produce small black spots (penetrating skin) or red spots (excoriations).

At even closer range the smoke from the gun can produce smoke stains on the skin, colouring the skin around the entry wound black. At even closer range than this the flame from the gunshot can burn the skin.

All these residues are collected and mapped and compared often with shooting experiments to determine firing range and gun type (each gun has its own distinct pattern of residue spread).

If the gun is fired at point blank on contact with the skin, a so called contact wound is produced. This is often stellate in shape, the flaps are caused by the pressure of air as it escapes around the gun, it can look like a blunt force injury so be careful in your description.

If the bullet penetrates a flat bone it can be easy to spot the entry and exit side from bevelling of the bone edge (the bone will be bevelled on the exit side of the bone and diameter of the hole as the entry side has a smaller diameter to the exit side. Exit wounds can be very messy and may sometimes look like a blunt force injury, sometimes if the victim is against a surface where the bullet exits eg. A wall, material from the wall behind can be found in the wound. 

In terms of treatment, GSWs must be treated with thorough debridement and delayed primary suture in the same way as battle injuries (future post). It must never be closed straight away! The debridement should be extra thorough taking extra care to remove fragments of clothing and soil from the wound. 

Clinically you can divide GSWs into low velocity and high velocity injuries. Low velocity injuries can cause little soft tissue damage as long as they remain stable (remember that oscillation and cartwheeling of the bullet will cause more damage). High velocity injuries act like a small explosion and many tissue planes are separated providing easy access for infections. There is often foreign material in the wound further enhancing chance of infection. 

St Emlyn's Emergency Medicine Blog

Shout out to this fantastic blog! Based out of the Manchester Royal Infirmary, St Emlyn's is an emergency medicine blog full of great insights into life as an EM doctor. There are lots of #FOAMed resources for those who are jumping on the social education bandwagon (a more modern version of medical education).
I particularly enjoyed this recent post about the risks of training in EM and why some Dr's quit and how to avoid those lows. @baombejp brings up the following points:

• Dont expect results too fast, take the SMART approach
• Dont fear failure, there are three ways you can react to a setback: you fly, you dive, you thrive
• With regards to the future find the right balance between competence and confidence when progressing and be careful of the unknown'unknowns (the things you dont know you dont know ha)
• Have a life! why have a job if you don't have a life
• There will be ups and downs, find someone to talk to about it

The blog is full of great posts, I enjoyed reading this morning about this consultant dealing with his junior knowing more than him and the following teaching tips. 

Acute Renal Failure and Acute Kidney Injury (ARF vs AKI)

If you look up the definition of acute renal failure (ARF) you will probably find this; "an abrupt and sustained decrease in renal function". Thats all very well but what do any of these words mean?! how abrupt? how long is sustained? renal function measured how? Whats more, over 35 different definitions of ARF are used in the literature with varying mortality and incidence rates. This post should hopefully clear everything up about ARF and AKI and give some tips about how to manage ARF and AKI.

First of all, scrap the term ARF, the term AKI is used now and reflects much better the fact that small decrements in organ function not resulting in organ failure are still clinically important! ARF is used for the last stage of AKI where the kidney actually fails and RRT (renal replacement therapy, for example hemodialysis) is needed. 

Diagnosis:

How do you know if a patient has AKI? look at serum creatinine and urine output!

There are two main ways for classifying AKI, the RIFLE criteria and the AKIN criteria, both perform equally well in studies, but I will use AKIN criteria because it is used by the KDIGO guidelines which most of this post is based on.

Picture above shows the AKIN criteria in the red box, as you can see you can divide AKI into three stages depending on the level of serum creatinine (sCr) or urine output (UO) (or directly place them into stage 3 if they are on RRT or anuric for greater than 12 hours). Stage 3 AKI is synonymous with ARF. 

So you have assessed your patients sCr and UO and find that he/she has an AKI. what do you do next?

AKI Management:

• monitor diuresis (bladder catheterise if not already catheterised)
• careful physical exam (pay attention to whether the patient is 'wet or dry', you should be careful giving fluids in a 'wet' pt, see later notes on pulmonary edema)
• monitor fluid balance
• arterial blood gases
• order labs: sCr, Na+, K+, Ca2+, Cl-, CBC, urine dipstick, BUN, 
• renal US (you are looking for the easy dx of obstruction, see etiology below)
• CXR (pulmonary edema?)
• avoid contrast agents if at all possible
• consider ICU if stage 2 and up
• avoid hyperglycemia
• careful drug review: 

1. discontinue nephrotoxic drugs (eg. vancomycin, gentamycin)
2. discontinue drugs that impair GFR autoregulation (NSAIDs, ACEi, ARBS(angiotension receptor blockers))
3. adjust dosage of drugs undergoing renal excretion (many antibiotics)
4. withhold exogenous potassium (look for K+ containing infusions (such as isolyte) that the patient may be on) and stop potassium sparing diuretics like spironolactone and eplerenone. 

AKI treatment:

Treatment is mainly directed at the underlying causes, for example if the cause is dehydration give fluids, if the cause is haemorrhage consider giving blood transfusion etc. immunosuppressants for vasculitis, discontinue drugs, relieve urinary tract obstructions....

note: No specific treatment for AKI actually exists but we have to manage all the complications well. 

AKI causes:

The causes of AKI are best divided into three main catergories

• pre-renal
• intrinsic (parenchymal)
• post-renal

Pre-renal AKI:

Basically anything that causes a drop in blood pressure low enough that the kidneys own auto-regulation is unable to preserve renal function. consider:

Volume loss: hemorrhage, dehydration, diarhhea, polyuria, burns

Sequestration of fluids (3rd spacing): pancreatitis, peritonitis, rhabdomyolysis

Blood pressure drop: any form of Shock, hypotensive medications 

(note that not all patients have the same capacity to autoregulate their renal filtration)

Intrinsic AKI:

diseases that affect the kidney directly, consider:

Arteries: thrombosis, embolic events

Pre-glomerular arterioles: Vasculitis, malignant hypertension, atheroembolism, DIC, eclampsia

Glomeruli: glomerulonephritis, thrombotic microangiopathy

Tubulo-interstitium: Acute tubular necrosis (ATN), crystalluria, cast nephropathy, contrast agents

(note that anything that can cause a sustained hypotension can damage the renal epithelium and cause ATN)

Post-renal AKI:

This is caused by an obstruction to the urinary tract, consider:

Bladder outlet obstruction: BPH, urethra stenosis, neurologic bladder

Ureter obstruction in pts with 1 kidney: stones, cancer, papillary necrosis

AKI Complications:

AKI patients can die of four main causes:

• Hyperkalemia
• Metabolic acidosis
• Fluid accumulation (pulmonary edema)
• Uremic syndrome

Hyperkalemia occurs when serum K+ is >5 mmol/l

Symptoms of hyperkalemia include: intestinal colic, diarhee, weakness/paralysis, arthymias

Hyperkalemia has a distinct ECG: flattened P waves, wide QRS, peaked T waves

(peaked T waves is the first feature to appear)

Metabolic acidosis is caused by the failure of tubular interstutium to excrete normal daily acid load. symptoms include: nausea and vomiting, abdominal pain, hyperventilation, hypotension

(note that acidosis may worsen hyperkalemia)

Fluid accumulation is quite often iatrogenic! careful with hydration. 

Uremic syndrome has many presentations and may cause: pericardial effusion, nausea and vomiting, malaise, confusion, seizures, non specific diffuse abdominal pain, ileus, a tendency to bleed (so called 'lazy' platelets). 

Mean Arterial Pressure (MAP)

I'm currently studying shock, its a huge subject and incredibly important topic in medicine. It doesn't matter what kind of doctor you are, you need to be able to deal with shock. MAP is very relevant in the state of shock.

MAP a great indicator of the perfusion pressure of the organs. Its kind of like an average blood pressure, so if its low there isn't much blood reaching the vital organs. As we all know, blood pressure has two components a systolic and diastolic component. So its not so easy to work out MAP or 'average' blood pressure.

There are some formulas that help (DBP = diastolic blood pressure, SBP = systolic blood pressure):

MAP = DBP + 1/3 (DBP-SBP)

MAP = 2/3 DBP + 1/3 SBP

There are many and quick search of wikipedia or on google will easily come up with many different formules, the two above are the simplest. (note: DBP - SBP is also called the Pulse Pressure).

A normal MAP in a healthy subject is around 90mmHg or in the range 70-110mmHg,
In the treatment of shock we are trying to get the MAP to around 65mmHg or maintaining it there.
(this is because a MAP above 60mmHg is considered enough to perfuse the organs. thus below 60mmHg you should start worrying about organ ischemia).

First Aid Saves lives! part one Airways

Just got back from a mandatory first aid course at work, being a medical student and having done first aid courses before, it was easy to think I already knew it all. I was surprised at how much I learnt from the experience. 
The first thing I learnt was some shocking statistics;

• Two thirds of people in the British public couldn't save a life in the event of an emergency.
• over a quarter of people who said they knew first aid would of done the wrong thing in an emergency (for example if someone was choking they would put their fingers in the persons throat to relieve the obstruction (pushing the obstruction further down))
• In the UK, less than one in ten will survive a heart attack while in Norway over 25% will, most likely due to the fact most people in Norway are able to perform CPR (First aid training being mandatory in Norwegian schools). 

I'll try an give a concise summary here about what was covered. also big thanks to Actual First Aid for the excellently run course. 

When approaching an emergency or an unconscious individual the mnemonic to use is:

DR ABC

D is for Danger. 

First, make sure its safe to approach, we dont want to generate another casualty for the ambulance to deal with. A classic example would be a car crash situation and oncoming traffic, a second crash?

R is for Response

You need to determine if the casualty is conscious, check this by asking a simple question."are you ok", perhaps they cannot respond verbally, so ask "can you open your eyes". if there is no response, you should call for help and contact the emergency services and move onto ABC. 

A is for Airway

The tongue is an incredible muscle, unlike the muscles in your arms and legs, the tongue is only attached at one point. The picture below highlights the tongue (purple) and its singular attachment at the bottom of the mouth in a cadaver. When someone loses consciousness the tongue relaxes completely and falls back slightly covering up the airway (not the thin route to the airway in the cadaver).(By the way its impossible to swallow your tongue, just try it).

The airway can be opened by gently tilting the head back by applying pressure to the forehead with your hand. HOWEVER, its possible in many situations that the casualty may have sustained a spinal or cervical spinal neck injury. In this case movements of the head and neck are to be avoided if there is any suspicion of neck injury. So how do you open the airway?
The best way to open the airway in this case would be by dislocating the jaw and bringing the jaw forward the so called 'jaw thrust' maneuver.
This is performed by placing three fingers behind the angle of the jaw close to the ear and with your thumbs applying pressure to the cheek bones below the eye, you pull the jaw forward and out so that the head doesn't move. (the movement of the jaw, pulls the attached tongue forward as well, allowing air to pass).

B is for Breathing
not breathing? you should consider CPR see part two...

C is for Circulation
no pulse? you should consider CPR see part two...

Pseudoaneurysms

Interesting case in the emergency theatres today. 40yr old male with a large hematoma in the left thigh. One week ago he underwent a cardiac procedure that required the use of an intra-aortic balloon pump.
Have an idea yet?
Insertion of an IABP is through a catheter in the femoral artery, if this puncture is misplaced or compression afterwards to close the wound is insufficient then the artery can continue bleeding into the thigh and form a pseudoaneurysm.
This chap had a pseudoaneurysm for exactly that reason, in fact you could see on doppler-ultrasound the hole was in the superficial femoral artery. The superficial femoral artery is a common origin of pseudoaneurysms because when you apply compression to the leg after cath lab or interventional radiology procedures for hemostasis, the femoral bone is not behind (as it would be for a standard common femoral artery puncture), so compression is ineffective.

What is a pseudoaneurysm?
Usually the result of injury to an arterial wall a pseudoaneurysm is an aneurysm lacking all three normal elements of an arterial wall. Pulsatile flow from the ruptured artery dissects the neighbouring tissues and forms a false lumen or sac containing the hematoma.

Risk factors: are any intra-arterial puncturing procedure, which increases in proportion to the size of catheter (larger catheters having higher rates of pseudoaneurysm formation). The risk is increased when the puncture site is not the common femoral artery eg. external iliac, superficial femoral and profunda femoral arteries.

How do you diagnose a pseudoaneurysm?
Most common presentation is pain and swelling in the groin area. Often the pain is disproportionate to the pain expected from the procedure. Large hematomas can compress neighbouring nerves and veins, and even cause skin necrosis.
Conduct peripheral pulse examination, ankle-brachial index and ultrasound scan of the area.
The best intial diagnostic test is a duplex ultrasound scan (7mhz linear probe). you can find and measure the diameter of the pseudoaneurysm neck.
If a doppler US scan cannot be performed the next step is a CT scan with contrast.

Management and treatment
So after support and resuscitation (a ruptured pseudoaneurysm can lead to catastrophic bleeding).
there are four main treatments:

1. Observation: for small pseudoaneurysms, less than 2cm. these will often spontaneously heal within a few weeks. keep monitoring with regular ultrasound scans. disadvantages include prolonged hospital stays and restricted activity.
2. US-guided compression: very variable success rates, the compression has to be maintained for at least 15minutes, aim for 20minutes. the probe can be used to target the pseudoaneuryms neck accurately. disadvantages include the fact that it not tolerated well and can be challenging. 
3. Percutaneous thrombin injection: guided by US thrombin is injected into the pseudoaneurysm cavity for immediate thrombosis. the real risk of embolism limits the procedure to pseudoaneurysms with a neck smaller than 4mm. often a well tolerated and successful procedure it does require anticoagulation therapy. 
4. Open surgical repair: Best for patients with complications or contraindicated to non-surgical management. open surgical repair allows direct visualization and control of the bleeding with suturing of the puncture site or patch angioplasty. hematoma can be evacuated and compression symtoms relieved. there are of course risks with any surgical procedure with  wound infction, lymphocele, radiculopathy and myocardial infarction topping the list. (make sure you check both sides of the artery).

So our patient had intially complained of a small thigh hematoma a few days after the cardiac procedure, he was infact in ITU with respiratory problems (complicated history). The surgeon had a look and since it was small and also considering the state of the patient, opted for the observation approach. so four/five days later the hematoma had expanded rapidly and considering the blood loss and size, open surgical repair was the best option. Operation went well, chap is doing fine. the hole was easily controlled with a controlled stitch and the hematoma evacuated from the anterior thigh and inguinal area. 

(pseudoaneurysm after arterial puncture to the superficial femoral artery)

Haematemesis

Haematemesis (vomiting blood) can present as either bright red in appearance (a medical emergency, suggesting an acute bleed) or a dark granular so called 'coffee grounds' (suggesting the bleeding is modest or has already ceased).

Causes of Haematemesis:

• Peptic ulcer disease: most common cause, often epigastric pain a well. Most often due to Helicobacter infection or NSAID use. 
• Upper GI malignancy: patient will often have fatigue, weight loss, anorexia and early satiety accompanying symptoms. 
• Varices: formed with portal hypertension when blood is trying to find routes to avoid the liver, most commonly with hepatic cirrhosis.
• Mallory-Weiss tear: characteristic history of forceful vomiting with haematemesis following (intial vomiting clear of blood). 90% of these will heal spontaneously.
• Gastritis/Duodenitis: consequence of Alcohol abuse or NSAID overuse. nausea and epigastric pain common.
• Oesophagitis: consequence of GERD. History of heartburn typically. 
• Dieulafoy’s lesion: developmental lesion, an unusually large (5-10mm) submucosal artery in the stomach wall. The pulsatility of which causes it to eventually erode through the stomach wall and perforate into the stomach. 
• Aorto-duodenal fistula: history of recent aortic surgery. 

Management, what to do:

The priority is resuscitation, patients with haematemesis may present in shock. So ABCDEs first. If a patient does present with shock or bright red haematemesis then after they are stabilised they need urgent upper GI endoscopy.
Get urgent CBC, U+E, coag screen, cross match and LFTs 
Varices have a high mortality rate and may be suggested by known chronic liver disease or characteristic signs if liver disease.
If patient has characteristic history of a Mallory-Weiss tear then endoscopy is not needed.
If active bleeding is not suspected and patient is stable, then take a full clinical history and exam. Suspect first gastritis, duodenitis or oesophagitis and pay attention to signs of malignancy.
If the diagnosis is not obvious consider inpatient endoscopy.