Paramedic Basics

- Fingertip injuries

Whilst not often life threatening, finger tip injuries are common and painful. Some will benefit from treatment at hospital, however it’s important that we only transport patients who actually require our services

BACKGROUND
📕 Most common in children < 5 years (exploring) and adults > 65 years
📕 Common mechanisms are crush (fingers in car door), laceration and amputation
📕 3:1 male to female incidence

ANATOMY
👉🏼 Nail plate - the part we commonly refer to as nail
👉🏼 Nail bed - the vascular structure that feeds the nail
👉🏼 Germinal matrix - the origin of the nail plate
👉🏼 Pulp - the flesh around the finger bone
👉🏼 Distal phalange - the bone making up the finger tip

COMMON PROBLEMS
🛠️ SUBUNGUAL HAEMATOMA
A collection of blood under the nail plate, can be quite painful due to pressure buildup. Usually described as the % surface area of the nail that the haematoma covers. Can be managed conservatively, with a bore hole (trephination) or nail removal. Haematomas > 50% suggest nail be laceration

🛠️ NAIL BED LACERATION
Lac impacting both the nail plate and nail bed. Infection and nail by growth disruption are both risks. Managed by removing the nail, delicately suturing the nail bed and returning the nail

🛠️ FRACTURE
Can occur with any fingertip injury, needs xray to rule out. Several types, notably a Seymour fracture, a serious finger fracture which impacts the growth plate in children

PARAMEDIC MANAGEMENT
🚑 Control haemorrhage
🚑 Analgesia
🚑 All paeds should be assessed at hospital to rule out Seymour fracture
🚑 Adults with subungual haematoma < 25% and controlled pain can manage with self care (analgesia, ice, elevation)
🚑 Haematoma 25 - 50% with controlled pain should be referred to GP/urgent care for review and possible trephination
🚑 > 50% subungual haematoma should be reviewed at hospital for nail bed repair
🚑 For all patients with controlled pain and no other injuries/reason for transport, consider alternative means of transport

- The relationship between the ECG, cardiac myocyte action potential and mechanical movement of the heart

This came up today whilst teaching, the difficulty bringing together these three different concepts and making them apply to the one patient

- ECG: P wave, PR segment, QRS complex, ST segment, QT interval and T wave
- Cardiac myocyte action potential: Phase 0, 1, 2, 3 and 4, the associated movement of sodium, potassium and calcium ions. [Note cardiac pacemaker action potential is not featured]
- Mechanical: atrial contraction and relaxation, ventricular contraction and relaxation, and the relation to a palpable pulse

The relationship between the ECG and mechanical activity is essential for all paramedics to understand. The relationship between the ECG and cardiac action potential is very important, especially if you want to give anti-arrhythmic drugs to the patient

Please excuse the quality as this was a quick mock up during class - I will try to make a clearer on and post in the future

- Chest Pain DDx

Chest pain is a common reason for calls to emergency services. In Victoria it makes up 9.4% of ambulance attendances. Whilst common, diagnosing chest pain can be challenging. Given that the causes range from trivial to life threatening, it is something that paramedics want to get right every time.

One study found the causes of chest pain as:
- non-specific: 46% [30 day mortality 0.5%]
- NSTEMI: 5.3% [1.3%]
- pneumonia: 3.8% [3.9%]
- stable angina: 3.5% [0.8%]
- unstable angina: 3.3% [1.3%]
- STEMI: 2.8% [7.0%]
- pulmonary embolism: 0.7% [3.2%]
- aortic pathologies: 0.2% [22.2%]

(Dawson et al, 2022)

Given the number of differential diagnoses, it is easy to feel overwhelmed or out of your depth. Some paramedics will suggest ‘just treat them all as cardiac’. Whilst pay off principle is legit, we don’t want to be blindly treating (and transporting!) every chest pain as cardiac.

Today’s whiteboard offers some clinical findings which will assist in pointing you into the right direction. Some are based off guidelines, whilst others are based of clinical experience/conventional wisdom. It’s also worth remembering that there are abnormal/atypical presentations of all conditions.

Paramedics can and should diagnose problems. By assessing the patient, their history and preceding events, it is often possible to get the diagnosis right without imaging/pathology. We can then work on treating and conveying the patient to the right hospital based off that diagnosis.

It is okay to change your mind or re-consider a diagnosis - that’s why we reassess!

Always treat the patient in front of you and try to do what’s best for them

- Critical Asthma

Around 11% of Australians live with asthma - that’s 2.8mil people! Asthma exacerbations can range from mild to critical, and in the worst cases can result in death. Between 3-10% of these people will have severe disease.

Critical asthma is a term which refers to the sudden onset of severe asthma - it’s a time critical emergency which can cause deaths. In 2016 a thunderstorm asthma event caused thousands to be hospitalized and led to 10 deaths. In response to that, and informed by the evidence gained a new CPG for treating critical asthma was developed

The flow chart here demonstrates the downward spiral of deterioration for patients with critical asthma. Increased WOB (slight difficult to see on the flow chart sorry!), muscle fatigue, decreased expiratory time and gas trapping leads to a repetitive cycle. Hypercapnia, hypoxia and haemodynamic compromise follow.

CARE OBJECTIVES
✅ Early administration of adrenaline (IM/IV) in patients not responding to nebulised therapy
✅ Utilise an obstructive ventilation strategy and allow permissive hypercapnia

PARAMEDIC MANAGEMENT:
🚨 Administer nebulised bronchodilators (treats bronchospasm)
🚨 Oral steroid (treats mucosal oedema - slower acting)
🚨 Maintain SpO2 > 92% (titrate the flow through the neb mask or use ETCO2 nasal prongs)
🚨 Administer IM Adrenaline (alpha/beta adrenergic action = bronchodilation, decreased mucosal oedema, increased venous return and cardiac output) to patients critically unwell or not responding to nebs
🚨 If no response to IM Adrenaline, administer IV Adrenaline
🚨 MICA can commence an Adrenaline infusion and BiPAP
🚨 If patient becomes unconscious - commence BVM ventilation with obstructive strategy

💔 ASTHMATIC ARREST 💔
- Allow 1/60 apnoea to release gas trapping
- Prepare for cardiac arrest management
- If still in arrest after 1/60: commence medical cardiac arrest
- If pulse returns with no BP: MICA administer IV Adrenaline and fluid
- If pulse returns with BP: treat as above for critical asthma

- Shoulder Dystocia

Shoulder dystocia is a time critical emergency which anyone who delivers babies needs to know about. Occurring when the baby fails to deliver because it’s shoulder is stuck, there is a short window to resolve SD before permanent damage or death can occur

INCIDENCE:
Occurs in 1% of all vaginal deliveries
Some correlation with baby’s size, however 50% of SD occurs in normal birth weight
Some predictive risk factors however 50% of SD have no risk factors

🚨 SO IF YOU’RE A PARAMEDIC YOU NEED TO BE ALL OVER THIS!

CLINICAL PICTURE
- head down delivery
- head delivered but not advancing
- head may be retracting (turtle sign)
- head to body time > 60 sec

PARAMEDIC MANAGEMENT
📞 Immediately request backup and commence specialist telehealth consult
🚨 Advise all on scene of SD, and inform mother
🦵 Position mum with buttock on edge of bed if possible, and provide *gentle* downward traction on the baby

If still not delivered, move through these manoeuvres

1️⃣ McRoberts Position
“Knees to nipples” - helps open up pelvis and increase pelvic outlet diameter

2️⃣ Suprapubic Pressure (while still in McRoberts Position)
Hands in CPR style grip, placed at a 45 degree angle to baby’s back. Apply constant pressure for 30 seconds (helps reduce bisacromial distance and rotate baby more oblique).

After 30 seconds, commence a gentle rocking motion to try and achieve the same goal.

3️⃣ Gaskin Position
“All fours” - helps release the posterior shoulder, which is sometimes the culprit. Be aware that whilst moving position baby may suddenly be released!

🛑 If these techniques are not successful, discuss with PIPER when to abandon the attempt and transport the patient. They may also direct you to perform additional maneuvers

PEARLS:
- practice practice practice these techniques, even if you don’t have access to a training mannequin
- communication to parents and other paramedics on scene is essential
- escalate care early!
- be prepared to perform resuscitation once baby is delivered
- don’t forget to monitor mum closely after delivery (consider a second crew!)

- Bowel Obstructions

Bowel obstruction is a common surgical emergency, being the underlying cause of 15% of abdominal pain presentations to US EDs. Its incidence is 100-500 per 100,000 people, with majority of cases occurring in patients who have had previous abdominal surgery

PATHOPHYSIOLOGY
🛑 the main cause of bowel obstruction in the developed world is adhesive fibroids (scarring) from prior surgeries
🛑 other causes include cancer, hernias, inflammatory disease processes, foreign bodies and pseudo-obstructions
🛑 the obstruction prevents movement of food through the gut, causing the proximal area to dilate whilst the distal section collapses
🛑 vomiting occurs, which can cause dehydration and electrolyte disturbance
🛑 the bowel swells, gut lining is disrupted and further fluid losses occur (third spacing)
🛑 if the bowel becomes strangulated, disruption of blood supply can cause ischaemia, infarction, perforation and sepsis

RISK FACTORS:
⚠️ prior abdo surgery
⚠️ cancer
⚠️ diverticulosis
⚠️ inflammatory bowel disease (eg Crohns)
⚠️ swallowed foreign body
⚠️ chronic constipation

MANAGEMENT
💉 IV access
💉 symptomatic management (analgesia, anti-emetic, fluids and antibiotics)
⚠️ keep the patient nil by mouth
🚑 transport to a hospital with surgical capability

- Intussusception

More than just a mouthful to say, intussusception is a potentially serious conditions effecting 1 in 2000 children annually in the US. When detected and treated early, prognosis is very good

PATHOPHYSIOLOGY:
- 90% of cases are idiopathic
- one part of the bowel is propelled into the next bit, causing a ‘telescopic bowel’
- usually the proximal bowel is lodged in the distal bowel, due to peristaltic (digestive) movement of the gut
- the stuck section of bowel can lose its blood supply, becoming ischaemic
- if left untreated, bowel perforation, necrosis and sepsis can occur

CLINICAL PICTURE:
- usually aged 2 months to 2 years, but can occur at any age (including adults)
- typically occurs around age 5 months
- boys more affected than girls (3:1)
- child appears very distressed and in pain, occurring episodically
- associated vomiting, lethargy, pallor
- sausage shaped mass may be felt over the right side of abdomen
- may initially have diarrhoea, which can lead to a misdiagnosis of gastroenteritis
- re**al bleeding / red currant jelly stool is a late sign

MANAGEMENT:
- nil by mouth in case surgery is needed and to reduce pain
- IN Fentanyl
- Ondansetron wafer
- if shocked, request MICA for fluid resuscitation (20mL/kg)
- transport to paed surgical hospital

PEARLS:
- intussusception usually isn’t associated with fever, whereas gastroenteritis is
- remember that patients may appear very well between episodes of pain - if not providing transport, ensure there is rigorous safety netting and referrals are in place
- the younger (or less verbal) the patient is, the more thorough your physical exam should be

Whiteboard Wednesday - Oxygen Induced Hypercapnia (Hypercarbia 🇺🇸)

After some interesting conversations recently, I thought we were well overdue to talk about why we use oxygen with caution in patients with chronic hypoxia/hypercapnia

First things first - hypoxic drive theory is not evidence based. If it does occur, it’s likely not a significant contributor to hypercapnia, but rather hypercapnia causes CNS depression and respiratory depression

So, how DOES adding oxygen cause carbon dioxide to rise??
Two mechanisms - ventilation/perfusion mismatch (75% responsible) and the Haldane effect (25%)

💨 V/Q Mismatch
People with chronic hypoxia (COPD, obesity, neuromuscular disease, cystic fibrosis, etc) have poorly ventilated sections of the lung
Pulmonary blood adjusts based on the amount of oxygen in the alveoli - this is adaptive as it ensures well ventilated alveoli are well perfused, and vice versa
Adding supplemental oxygen reverses this hypoxic vasoconstriction - increasing perfusion to poorly ventilated areas (dead space) and reducing perfusion to well ventilated areas (shunting)
This V/Q mismatch reduces gas exchange, leading to CO2 retention

🩸Haldane Effect
Carbon dioxide is partly transported in blood attached to hemoglobin molecules. CO2 has greater affinity for deoxygenated Hb molecules than oxygenated Hb
For patients with chronic hypoxia, a relatively larger amount of CO2 is “stored” in red blood cells, rather than being dissolved in blood
When excessive O2 is administered, it causes a shift of CO2 off the Hb and dissolving into blood
For patients already acutely short of breath, they cannot increase their minute ventilation to ‘blow off’ the CO2

How to manage/prevent this?
- avoid excessive oxygen administration, target SpO2 88-92% (causes reduced mortality in COPD patients!)
- give bronchodilators/steroids as needed
- nebulise on room air if available. If using O2, use 8L/min and cease as soon as meds given
- high concentration O2 devices (non-rebreather) can be used for severe hypoxia, but should be downgraded to nasal prongs as soon as possible
- ensure adequate ventilation, consider MICA backup for NIV in severe cases

- Different IV Fluids

If your service is anything like mine, we’ve been relying on good old fashioned 0.9% Sodium Chloride (Normal Saline or “pasta water”) for quite a while

As a cheap, compatible, isotonic fluid, it is ubiquitous around the globe. However issues with supply means that we are now facing an international shortage of our favourite salty water

In response, Ambulance Victoria has introduced two additional fluids to service - Compound Sodium Lactate (Hartmann’s) and Plasma Lyte 148

Both are so-called ‘balanced crystalloids’, as they have electrolytes dissolved in them to more closely mimic blood plasma. Whilst they will have broadly the same indications as Normal Saline, there are a few nuances to be aware of

💧0.9% Sodium Chloride
- should be saved for patients with TBI, as it may be associated with lower mortality than balanced crystalloids
- avoid using 500mL/1000mL bags to draw up flushes (use ampoules)
- avoid hanging ‘just in case’ or TKVO

💧CSL
- not compatible with blood products (causes coagulation)
- not compatible with Ceftriaxone (causes calcium precipitation). The effect is so significant that they cannot both be given to infants < 28 days, even via separate lines. For patients older than 28 days, they can be co-administered but NOT via the same line
- can’t be used to reconstitute powdered medications due to lack of research

💧Plasma Lyte 148
- incompatible with Amiodarone and Propofol
- can’t be used to reconstitute powdered medications due to lack of research

My general approach?
1️⃣ Use Normal Saline for head injured patients

2️⃣ For all other patients older than 28 days, use Hartmann’s.
If not available, then use Plasma Lyte 148

3️⃣ For patients < 28 days requiring fluid resuscitation, use Plasma Lyte 148.
My thought here is that they will likely receive antibiotic cover and we don’t want to limit options

💰 Also worth noting that Plasma Lyte 148 is more expensive than Normal Saline and Hartmann’s. Although money isn’t everything, if the patient gets the same effect then we have a job to spend healthcare resources wisely

- Head Injury

You all know how to look after the big scary TBI (if not, there’s a whiteboard for that!) But what about the minor head bump, the concussion… what do we do with them?

Did you know that not all head injured patients need to go to hospital? You’ve probably done this in your own practice - toddler who rolls off the couch is usually fine to stay at home, but that same toddler who falls from height presents more risk

This whiteboard (based off the Ambulance Vic CPG) looks at the risk stratification of adult and paediatric head injuries. Starting from the left, we’re looking at High Risk criteria. These are the criteria you already know - GCS < 13, penetrating head injury or meeting 5HEDS. Note that multiple vomits and seizure at time of impact are NOT high risk criteria for paediatrics, as these tend to occur even in moderate head injury. High Risk patients are trauma time critical and should be transported to a MTS in < 60 min. If you’re outside that distance, consider HEMS or a closer hospital (preferably with neurosurg)

If there’s no High Risk criteria, consider the Moderate Risk. These are more subtle assessment finding, high risk mechanism of injury or risk factors for serious injury. Patients with moderate risk usually require hospital assessment, with most adults receiving a CT brain. Some of these patients may be suitable for VVED consult

When there are no high or moderate risk criteria, the patient is Low Risk. These patients can generally self care at home, and should be sent a health information sheet. Safety netting, including advice about when to call back is essential to a good outcome