Article 8
Normobaric Oxygenation as a First-Aid Measure
In Decompression Sickness
by:
Lim Ju Boo
Regional Staff Officer (Training Division)
St. John Ambulance Malaysia
My youngest sister, a Singaporean, often likes to come up here to Malaysia to Tioman Island, and other nearby islands to scuba dive to some depths. Another friend of mine, an astronomy enthusiast also does the same, and he also does some star gazing in the outreaches of some dark islands where the skies are clearer after the dive. Both of them complain (although my sister has never told me directly, except through her husband) of some joint and muscular pains at night each time they scuba dive. Their complain is unbiased, since my sister and my friend do not know each other, and they do separate diving, so they may be accepted as unbiased observation in a case study. I suspect their *symptoms (see foot-notes) is an indication of a condition called ‘bends’.
Perhaps at this point I should explain what bends are, since I suspect it was not taught in the St. John Ambulance (SJAM) first-aid classes (not that I know of). It was definitely not taught in the Red Crescent first-aid course nor in the First Responder course did I attend. I know it was not taught because I was at ‘concert pitch’ (keyed-up, tuned in to hear and record every note or word, right or wrong), on what the instructors said. I suspect not many first-aiders know what ‘bends’ is, let alone the first-aid for this condition. So I shall begin by explaining what bends is all about, before I proceed with a discussion on the subject.
Bends, used to be called caisson disease, medically called ‘decompression sickness’, is the result of gas mixtures (chiefly the inert, less soluble nitrogen) forming gas bubbles in the tissues of diver ascending too rapidly to the surface. The solubility of gas mixtures (compressed air carried in the cylinders by the diver) varies at various pressures as the divers ascend to the surface after a dive. At depths, divers accumulate large quantities of inert gas (chiefly nitrogen, - 78% in the compressed air) in their tissues. Normally the amount of gas can be held dissolved in the tissues such blood and body fat as the diver descends, the higher the pressure, the greater the solubility. Because of differences in solubility with partial pressures as the diver ascends to the surface, the less soluble ones will bubble out in the body tissues first. This is specially true as the pressure decreases rapidly when the diver makes a rapid ascend, leaving little time for the blood to clear the less soluble gasses. This is like opening a bottle of beer, and you see all the bubbles of carbon dioxide spewing out from the bottle. Partial pressure of a gas is the product of the percentage of a gas in a gas mixture, multiplied by the total pressure in that mixture.
In decompression sickness, bubbles may block blood vessels, causing various symptoms, from impairment of the nervous systems – muscular weakness, paraesthesia, dermatomal numbness and pain, paraplegia, bowel and bladder disturbances, CNS (Central Nervous System) changes, visual disturbances, or dys-coordination and balance due to gas bubbles within the labyrinth (semicircular canals, vestibules, cochlea) of the ears causing vestibular damage (‘the staggers’). More seriously, is a crushing chest-pain (angina pectoris) from gas bubbles forming in the coronaries of the heart, and circulation to the lungs (pulmonary gas embolism). There maybe dyspnoea (‘the chokes’). If the gas is released into muscles, skin and lymphatics, it may cause pain in limbs, pruritus (itchiness), marbled skin, painful lymph nodes, lymphoedema (fluid accumulation in tissues due to obstruction of lymph vessels). Some of them, especially if they involve the heart or brain, can cause sudden death. All these can be avoided if the diver ascends slowly by allowing the un-dissolved gases to escape slowly via the blood to the lungs.
In scuba-diving and hyperbaric medicine, the victim is placed in a recompression chamber. Pressure within the chamber is raised by pumping in air. This procedure forces the bubbles to re-dissolved into the tissues, and the victim becomes asymptomatic (no symptom) again. The pressure within the chamber is then slowly decreased to release the gas slowly to escape to the lungs via the blood. So far, so good! But such procedure can only be carried out at certain centers equipped with recompression chambers, and I understand there are only a few in this country. The main centre is at the Naval Hospital in Lumut where the recompression chamber may be filled with compressed air or pure oxygen up to 2 atmosphere pressures. The other two centers for hyperbaric therapy are at Kuantan and Labuan. The one at Lumut treats not only bends, but also other medical conditions where hyperbaric oxygenation is indicated, such as in gangrene, in AMI (acute myocardial infraction), and in carbon monoxide poisoning. The therapy normally last for 1 –2 hours. The treatment is very expensive because pure compressed oxygen is used, and imagine you have to fill up the whole chamber with it under twice the atmospheric pressure. The chamber is sufficiently large to accommodate not only the victim, but also medical personnel inside. The other two centers in Kuantan and Labuan are less sophisticated, and they are used only for the treatment of decompression sickness.
So what do we do? What is the first-aid for bends I mean? Of course I understand what you are going to say since you were not taught about bends in the first aid classes. The simplest answer to give is to bundle up the victim to such a centre. That’s the simplest thing. But what is the immediate (first-aid) measure? Now that we know what bends is all about, we are now in a better position to critically discuss the first-aid treatment at a more advanced level. Can we just give oxygen to increase the partial pressure? Yes you may, but….
Most divers and diving medicine specialists know that the application of normobaric (at normal atmospheric pressure) oxygen as FIRST-AID (before transport to a hyperbaric centre) after a bubble disease incident is highly effective. However, as yet certain technical difficult acted as a constraint in using normobaric oxygen at the site of the accident. Administering pure oxygen through nasal cannula, or through an ill-fitting face mask, or even through a nonrebreather mask is only partially helpful, but not totally useful. That still won’t solve the problem of getting the other gasses out. Remember what we discuss about solubility of gasses and their partial pressure in our above introduction? Now you can guess why ill-fitting oxygen mask is unsatisfactory. Some work has already been done to overcome this difficulty by a newer first-aid technique. To make it more effective, any first line therapy of bubble disease should follow three main principles:
1. Maximal partial pressure of inhaled oxygen, abbreviated as PO2 (oxygen and other gas mixture in a cylinder, each exert part of the total pressure), i.e. 100 kpa (about 750 mm Hg, or 1 atmospheric pressure) in normobaric, and 280 kpa in hyperbaric (say inside a compression chamber if available, or go back to the sea again and administer the oxygen under the sea where the pressure is higher) conditions; minimal partial pressure of inhaled nitrogen which ideally be near zero
2. Immediate start of first-aid therapy, if possible at the diving site itself, but not later than 2 hours after the onset of the first symptoms.
3. For an efficient normobaric oxygenation (100 %), the standard design without oxygen reservoir is obsolete, for it offers at most 40 % oxygen to the lungs. Currently the following technical approaches for an efficient normobaric oxygenation are available : open one-way systems with tightly fitting mask and oxygen reservoir bag (Ambu or Leardal bag, etc); open system on demand regulation and tightly fitting mouth piece (SCUBA, or Bird-respirator type); closed systems with CO2 absorber (oxygen rebreathing diving gear).
Any first-aid oxygen gear, or an ambulance fitted with the closed system is a genuine technical advance, because it needs 15 times less oxygen than open system (about 90 liters oxygen for a 3-hours oxygenation run). Such an apparatus is thus of light weight, far less cumbersome, and of course highly efficient. Importantly, the first-aid should start immediately at the site of the mishap and maintained throughout the period of transport to the nearest hyperbaric oxygen unit. Some work on this advancement in first-aid for compression sickness was conducted in Germany by Wendling, J., and was published in a journal on Sports Medicine (1).
Perhaps I should warn my youngest sister who never tells me anything, about decompression sickness. But I believed she knows about this, as she is a qualified scuba diver. And perhaps to my argumentative and talkative astronomy-scuba diving friend as well, I should also give this first-aid advice (provided he doesn’t argue with me until I sometimes have to put my head down, closed my eyes, and cover my ears with both my hands to be nullified).
Still on the subject on decompression sickness, here is another critical comment. For several years now, a controversy arises as to how to position a patient after a decompression accident with acute gas embolism (the pathology I have already explained). The usefulness of the so-called Trendelenburg position, based on experimental evidence gathered on dogs , has recently been challenged. The basis assumption was that cerebral embolism may be reduced by the hydrostatic effect of putting the head below the body’s centre of gravity. This position however requires a lot of technical resourcefulness, and may be difficult without an adjustable stretcher , and this often delayed the first therapeutic intervention, say at the site of the incident. Recent advances in experimental research shows that, contrary to the old theory, positioning the head below feet level increases the intra-cranial pressure (I think this is common sense reduction, due to pooling effect of blood flow and CSF), injuring the blood-brain barrier, even when performed under hyperbaric oxygen therapy. (My commonsense tells me there is there is no need to conduct an experiment to demonstrate this!).
Now a wide consensus has emerged from a study which should be communicated to all paramedics, first responders and first-aiders so that no more time is wasted fighting and quarrelling over the question how to position the patient by unduly complicated means and angles. Summarizing a report which I read, the current recommendations asks for laying the injured diver horizontally on his/her back, or sideways, if he/she is concious. The recommendation is that it is far more important to control its vital functions, give first-aid, administer oxygen in closed circuit (already discussed above), and shorten as much as possible, the transport time to the nearest hyperbaric therapy centre (Lumut Navy Hospital, or the General Hospitals in Kuantan or Labuan) Good luck to you all first-aiders who may have to deal with
scuba divers. Hope the paramedics will also read this (2).
Sunday, April 25, 2010
Article 7
Effect of External Cervical Spine Immobilization
on Intracranial Pressure
by:
Lim Ju Boo
Following my discussion on pelvic injuries, I would now turn a little to injuries to the superior part of the body - the head. A head injury is a common cause of death in MVA (motor vehicle accidents) in Malaysia. The pathophysiology in head injuries, besides other features like subpial and subarachnoid haemorrhages, and extradural haematoma, there is also a rise in the intracranial pressure. But we are not going to discuss about bleeding or other damages to the brain as right down I am concentrating and commenting on a paper I read on the application of external cervical spine immbolisation and intracranial pressure. But before I can do this, let me briefly explain what intracranial pressure is all about?
Intracranial pressure or ICP is the pressure of the cerebrospinal fluid (CSF) in the subarachnoid space between the skull and the brain. The pressure is normally the same as that found in during a lumbar puncture. There are many causes of elevated ICP after head injuries. Among the causes are:
• Haematoma
• Focal cerebral oedema associated with contusion or haematoma
• Diffused oedema after ischaemia (cytotoxic)
• Generalized or diffuse brain swelling (‘brain enlargement’)
• Obstruction of the cerebrospinal fluid circulation (rarely)
We now ask, what happens when the pressure within the skull occupied by the cerebrospinal fluid begins to rise following a head injury or in some major pathologies (such as in Reye’s syndrome in children). Once we understand this pathophysiology, we are ready to proceed to discuss its clinical importance in head injuries, before proceeding even further in discussing a paper by Kuhnigh and his colleagues.
Monro-Kellie Doctrine:
In a dogmatic teaching by a Scottish anatomist, Alexander Monro, Jr. (1733-1817), as far back as in 1783, and another Scottish anatomist George Kellie in 1824, they came out with a theory linking ICP and cerebral blood flow. Munro was also the President of the Royal College of Surgeons, and also a Professor of Physics (surprisingly), Anatomy and Surgery at the University of Edinburgh. He made a number of observations in his publication called ‘Observations on the Structure and Function of the Nervous System’ (1). Both of them advanced a dogmatic teaching, what is now known as the Monro-Kellie Doctrine, which states that since the cranial cavity is a closed rigid box, and that therefore a change in the quantity of intracranial blood can occur only through a displacement or of a replacement by cerebrospinal fluid. Briefly, that means when there is a rise in the intracranial pressure (intracranail hypertension) due to an accumulation of CSF, there would be a compensatory decrease in the blood flow to the brain to maintain normal ICP. The original doctrine was simple as it did not take into account the CSF or the spinal portion of the craniospinal compartment. Other researchers such as Burrows, Weed, Flexner and McKibben (3, 4) later modified the original doctrine. They established a reciprocal and compensatory relationship between blood flow and the volume of CSF. An increased in ICP naturally will decrease the cerebral perfusion rate and a resultant cerebral ischemia. A declining perfusion rate likewise is counteracted by the body by a rise in the mean arterial pressure. If the ICP continues to rise, the arterial pressure will also rise in respond, with a subsequent drop in the pulse rate and an increase in the respiratory rate. This respond, due to any space-occupying lesion (say a brain tumor, blood clots, generalized compression due to hydrocephalus, meningitis and subdural haemorrhage) is called Cushing’s syndrome, named after a U.S. neurosurgeon, Harvey W. Cushing (1869-1939).
Using animal models Cushing, in 1902 was able to show that the ICP rises slowly initially, and more rapidly as the volume increases (2). This compensatory mechanism can only go on up to a critical point until the built-up of ICP can no longer be compensated, and the continued ischemia (blood supply insufficiency due to ICP compression or tamponade effect) will injure the brain further, leading to hypoxia, and ultimate death. Intracranial hypertension if excessive can also cause herniation (prolapse) of the brain by forcing portions of the brain downwards through the foraman magnum (large hole at base of skull that transmit the medulla oblongata), and obviously this is going to damage the brain even more.
This is briefly what Monro-Kellie Doctrine is all about, and how this patho-physiological event, eventually becomes one of the causes of death in a head injury. An understanding of this mechanism makes it clearer for us to comprehend the seriousness of ICP elevation (IC hypertension) in head injury patients, besides other types of injuries to the brain of course. With that brief explanation and introduction, I am now more confident and prepared in trying to explain to my readers the importance of an elevated ICP, and a paper I have just read in connection with applying a neck collar. This is summarized below.
ICP link:
ICP in A link between an elevated ICP and the application of a cervical collar has been a suspected previously. This was investigated by a team of German neurosurgeons in the 1993 led by Kuhnigk et al. (5). The team measured the ICP in 18 patients with severe head injuries in the neurosurgical intensive care unit before and after placement rigid collar for cervical spine immobilization.
The purpose of the study was to determine whether the rigid collars, commonly use for the prevention of cervical spine movement during transport by paramedics, first responders and first-aiders to a treatment facility could lead to an increase in ICP ? Patients who had an *epidural transducer (An epidural transducer is an electronic device, fitted with baro (pressure) sensors or gauge that measures ICP within the cranial cavity, namely the outer membrane (dura) and the brain tissues deeper down, including the pressure inside the ventricles, if a separate intraventricular catheter is inserted in place) were studied, and their ICP recorded during the placement of either the Spieth cervical collar (n = 12) [ in scientific language and for statistical analysis, ‘n’ stands for the number (population) in a case study. In this case there were 12 patients being studied], or the Philadelphia cervical collar (n = 6). The baseline ICP was 17.0 +/- 6.1 mmHg (mm Hg means millimetres of mercury) versus 17.7 + / - 6.4 mm Hg 10 minutes after placement of the cervical collar.
Five minutes after removal, the ICP was 17.2 +/- 5.9 mmHg. No (statistically) significant changes in ICP could be demonstrated during this study. Placement of the cervical collar is a simple and practical measure to immobilize the cervical spine during rescue, and during the transport of intubated and ventilated patients. Its risk of increasing the ICP appears to be low even in patients with severe head injuries.
So there we are, we see how medical research of this sort (although only a very small study) can come to the aid of first-aid itself, and dispel our fears of applying a collar on trauma victims with head injuries as is usually practiced by paramedics, first-responders and first-aiders and even in the emergency room of a hospital. (By the way you might be wondering what the normal ICP is? Well, the normal ICP is about 10 mmHg. But it can go up to as high as 70 mmHg. in certain pathological conditions. The CSF which is largely responsible for the ICP, circulates over the entire brain and central nervous system at a rate of about 500 ml/day, and is formed at a rate of 0.4 ml./minutes. With this cycle, the CSF is renewed 4 – 5 times daily.)
* Foot-note:
The current devices in use in the neurological wards of hospitals for measuring ICP involve invasive procedures. The latest is a non-invasive modality, and is described in one of journals I received a month ago from the Royal Society of Health as a Fellow of The Royal Society of Health). The non-invasive work was done by Pension and Allen (6).
References:
1. Monro, A. Observations on the Structure and Function of the Nervous System. Edinburgh (1783). Creech and Johnson.
2. Cushing, H. Some Experimental and Clinical Observations Concerning States of Increased Intracranial Tension. Am J Medical Sciences. (1902), 124, 375-400.
3. Weed, L.H; Flexner, L.B. The Relationships of the Intracranial Pressures. Am J Physiology. (1933). 105, 266 – 272.
4. Weed, L.H; McKibben, P.S. Experimental Alteration of Brain Bulk. Am. J Physiology (1919). 48, 531 – 558.
5. Kuhnigk, H; Bomke, S; Sefrin. P. Aktuelle Traumatol. (1993, Dec.), 23 (8) : 350 – 3.
6. Penson, R.P. and Allen, R. Intracranial Pressure Monitoring by Time Domain Analysis. Journal of Royal Society for Promotion of Health. (1998, October). 118, No. 5. 289 – 294.
Effect of External Cervical Spine Immobilization
on Intracranial Pressure
by:
Lim Ju Boo
Following my discussion on pelvic injuries, I would now turn a little to injuries to the superior part of the body - the head. A head injury is a common cause of death in MVA (motor vehicle accidents) in Malaysia. The pathophysiology in head injuries, besides other features like subpial and subarachnoid haemorrhages, and extradural haematoma, there is also a rise in the intracranial pressure. But we are not going to discuss about bleeding or other damages to the brain as right down I am concentrating and commenting on a paper I read on the application of external cervical spine immbolisation and intracranial pressure. But before I can do this, let me briefly explain what intracranial pressure is all about?
Intracranial pressure or ICP is the pressure of the cerebrospinal fluid (CSF) in the subarachnoid space between the skull and the brain. The pressure is normally the same as that found in during a lumbar puncture. There are many causes of elevated ICP after head injuries. Among the causes are:
• Haematoma
• Focal cerebral oedema associated with contusion or haematoma
• Diffused oedema after ischaemia (cytotoxic)
• Generalized or diffuse brain swelling (‘brain enlargement’)
• Obstruction of the cerebrospinal fluid circulation (rarely)
We now ask, what happens when the pressure within the skull occupied by the cerebrospinal fluid begins to rise following a head injury or in some major pathologies (such as in Reye’s syndrome in children). Once we understand this pathophysiology, we are ready to proceed to discuss its clinical importance in head injuries, before proceeding even further in discussing a paper by Kuhnigh and his colleagues.
Monro-Kellie Doctrine:
In a dogmatic teaching by a Scottish anatomist, Alexander Monro, Jr. (1733-1817), as far back as in 1783, and another Scottish anatomist George Kellie in 1824, they came out with a theory linking ICP and cerebral blood flow. Munro was also the President of the Royal College of Surgeons, and also a Professor of Physics (surprisingly), Anatomy and Surgery at the University of Edinburgh. He made a number of observations in his publication called ‘Observations on the Structure and Function of the Nervous System’ (1). Both of them advanced a dogmatic teaching, what is now known as the Monro-Kellie Doctrine, which states that since the cranial cavity is a closed rigid box, and that therefore a change in the quantity of intracranial blood can occur only through a displacement or of a replacement by cerebrospinal fluid. Briefly, that means when there is a rise in the intracranial pressure (intracranail hypertension) due to an accumulation of CSF, there would be a compensatory decrease in the blood flow to the brain to maintain normal ICP. The original doctrine was simple as it did not take into account the CSF or the spinal portion of the craniospinal compartment. Other researchers such as Burrows, Weed, Flexner and McKibben (3, 4) later modified the original doctrine. They established a reciprocal and compensatory relationship between blood flow and the volume of CSF. An increased in ICP naturally will decrease the cerebral perfusion rate and a resultant cerebral ischemia. A declining perfusion rate likewise is counteracted by the body by a rise in the mean arterial pressure. If the ICP continues to rise, the arterial pressure will also rise in respond, with a subsequent drop in the pulse rate and an increase in the respiratory rate. This respond, due to any space-occupying lesion (say a brain tumor, blood clots, generalized compression due to hydrocephalus, meningitis and subdural haemorrhage) is called Cushing’s syndrome, named after a U.S. neurosurgeon, Harvey W. Cushing (1869-1939).
Using animal models Cushing, in 1902 was able to show that the ICP rises slowly initially, and more rapidly as the volume increases (2). This compensatory mechanism can only go on up to a critical point until the built-up of ICP can no longer be compensated, and the continued ischemia (blood supply insufficiency due to ICP compression or tamponade effect) will injure the brain further, leading to hypoxia, and ultimate death. Intracranial hypertension if excessive can also cause herniation (prolapse) of the brain by forcing portions of the brain downwards through the foraman magnum (large hole at base of skull that transmit the medulla oblongata), and obviously this is going to damage the brain even more.
This is briefly what Monro-Kellie Doctrine is all about, and how this patho-physiological event, eventually becomes one of the causes of death in a head injury. An understanding of this mechanism makes it clearer for us to comprehend the seriousness of ICP elevation (IC hypertension) in head injury patients, besides other types of injuries to the brain of course. With that brief explanation and introduction, I am now more confident and prepared in trying to explain to my readers the importance of an elevated ICP, and a paper I have just read in connection with applying a neck collar. This is summarized below.
ICP link:
ICP in A link between an elevated ICP and the application of a cervical collar has been a suspected previously. This was investigated by a team of German neurosurgeons in the 1993 led by Kuhnigk et al. (5). The team measured the ICP in 18 patients with severe head injuries in the neurosurgical intensive care unit before and after placement rigid collar for cervical spine immobilization.
The purpose of the study was to determine whether the rigid collars, commonly use for the prevention of cervical spine movement during transport by paramedics, first responders and first-aiders to a treatment facility could lead to an increase in ICP ? Patients who had an *epidural transducer (An epidural transducer is an electronic device, fitted with baro (pressure) sensors or gauge that measures ICP within the cranial cavity, namely the outer membrane (dura) and the brain tissues deeper down, including the pressure inside the ventricles, if a separate intraventricular catheter is inserted in place) were studied, and their ICP recorded during the placement of either the Spieth cervical collar (n = 12) [ in scientific language and for statistical analysis, ‘n’ stands for the number (population) in a case study. In this case there were 12 patients being studied], or the Philadelphia cervical collar (n = 6). The baseline ICP was 17.0 +/- 6.1 mmHg (mm Hg means millimetres of mercury) versus 17.7 + / - 6.4 mm Hg 10 minutes after placement of the cervical collar.
Five minutes after removal, the ICP was 17.2 +/- 5.9 mmHg. No (statistically) significant changes in ICP could be demonstrated during this study. Placement of the cervical collar is a simple and practical measure to immobilize the cervical spine during rescue, and during the transport of intubated and ventilated patients. Its risk of increasing the ICP appears to be low even in patients with severe head injuries.
So there we are, we see how medical research of this sort (although only a very small study) can come to the aid of first-aid itself, and dispel our fears of applying a collar on trauma victims with head injuries as is usually practiced by paramedics, first-responders and first-aiders and even in the emergency room of a hospital. (By the way you might be wondering what the normal ICP is? Well, the normal ICP is about 10 mmHg. But it can go up to as high as 70 mmHg. in certain pathological conditions. The CSF which is largely responsible for the ICP, circulates over the entire brain and central nervous system at a rate of about 500 ml/day, and is formed at a rate of 0.4 ml./minutes. With this cycle, the CSF is renewed 4 – 5 times daily.)
* Foot-note:
The current devices in use in the neurological wards of hospitals for measuring ICP involve invasive procedures. The latest is a non-invasive modality, and is described in one of journals I received a month ago from the Royal Society of Health as a Fellow of The Royal Society of Health). The non-invasive work was done by Pension and Allen (6).
References:
1. Monro, A. Observations on the Structure and Function of the Nervous System. Edinburgh (1783). Creech and Johnson.
2. Cushing, H. Some Experimental and Clinical Observations Concerning States of Increased Intracranial Tension. Am J Medical Sciences. (1902), 124, 375-400.
3. Weed, L.H; Flexner, L.B. The Relationships of the Intracranial Pressures. Am J Physiology. (1933). 105, 266 – 272.
4. Weed, L.H; McKibben, P.S. Experimental Alteration of Brain Bulk. Am. J Physiology (1919). 48, 531 – 558.
5. Kuhnigk, H; Bomke, S; Sefrin. P. Aktuelle Traumatol. (1993, Dec.), 23 (8) : 350 – 3.
6. Penson, R.P. and Allen, R. Intracranial Pressure Monitoring by Time Domain Analysis. Journal of Royal Society for Promotion of Health. (1998, October). 118, No. 5. 289 – 294.
Article 6
Pelvic Trauma: A Diagnostic
And Therapeutic Challenge
Lim Ju Boo
There was another very short summary statement as a cross reference from some papers (‘papers’ means technical papers from proper journals, and does not mean (news)papers please) I was flipping over last evening, published by Maurer in 1993. He said that it was shown that patients with pelvic trauma often have other multiple injuries that cause special problems (1). Well, I thought about this short, but important statement of his, and I decided that I should write and expand on this subject a little more here.
Crush injuries of the pelvis is commonly seen in about 5% of MVA (motor vehicle accidents) fractures in Malaysia (2). There may be also resultant pelvic fractures from vertical force applied by a fall from a height, the transmission of impact energy anterior-posteriorly, and vice-versa (AP/PA/AP), or laterally from a motor vehicle onto a pedestrian. Injuries to the pelvis can give rise to a number of complications, and they include:
Urogenital:
• Intraperitoneal and extraperitoneal rupture of the bladder
• Rupture of the penis and membranous urethra
Vascular:
• Damage to major vessels
• Massive haemorrhage from retropelvic vascular tear involving the iliac, lumbar, and other smaller arteries (blood loss from 1-4 litres)
• Ecchymosis (bruising and bleeding under the skin) may spread high up into pelvic cavity
• Disemination of intravascular clots
• Consumptive Coagulopathy
Neurological:
• Sciatic nerve damage
• Lumbosacral plexus involvement
Intestinal:
• Paralytic ileus (more common)
• Small intestine, colon and rectum (less common)
Others:
• May also involve extensive tear to the liver, spleen, pancreas, heart, lungs, and great vessels, spinal cord and extremities.
The major cause of mortality and morbidity in pelvic fractures may be due to massive haematoma and blood loss (up to 4 litres) from the damaged retropelvic arteries, especially in pelvic diastasis (diastasis means separation of bones at the epiphysis or joints, not amounting to a fracture), e.g. in ‘open book’ fracture of the pelvis where the symphysis pubis is opened out with appreciable sacro-iliac disruption). In major pelvic fractures where there is extensive bleeding, the chances of the casualty going into hypovolaemic shock are real. In such cases, the priority in first-aid is to immobilize the pelvic bone, and prevent shock (Trendelenburg’s position if necessary). If there are resulting haemorrhage shock, the application of anti-shock garments such as MAST suits. (MAST stands for Military (or Medical) Anti-Shock Trousers) can be one of the initial emergency first-aid treatment (to be done by paramedic or first responder if you like) prior to reduction (reduction is a surgical term to mean restoration to normal position) with external fixateur, and massive blood transfusion in a hospital. However the application of MAST or Pneumatic Antishock Garment (PASG) as advocated by some authorities is not without disadvantages and complications. Surprisingly, it has limited use in hypotensive trauma as shown by Mattox, et al. (3). Although, useful as a splint, by its tamponade effect, but it may also elevate intra-abdominal pressure, and hence may also raise intrathoracic pressure. This would cause resulting in difficulties with ventilation, cardiovascular and renal dysfunction as shown by Cullen, et al (4). In order to overcome the problem, a number of pelvic clamps and devices have been tried to reduce, compress, and immobilize the posterior fragments in a pelvic fracture, thus limiting further movement, tear and bleeding from bone fragments as reported by Ganz et al (5). Moreover, if pelvic fractures involve the long bones as well, there is also the risk of fat emboli (Fat Embolism Syndrome) especially in young adults, in whom fat globules from the long bones of the lower extremities (legs) may enter the lungs causing ARDS (Adult Respiratory Distress Syndrome). However all of these clamps require general anaesthesia for their application which in itself may cause complications in the unstable patient.
One special pelvic clamp device to address the massive bleeding, usually originating from hypogastric arterial involvement, associated with pelvic fractures, was invented by none other than Mr (Dr) Abu Hassan Asaari Abdullah, the Chief Traumatologist and Head of the Department of Emergency Medical and Trauma Services of Kuala Lumpur Hospital. This simple device does not require general anaesthesia for its application, and the application is so simple, it makes it possible for all paramedics, first-responders and first aiders to use it. It is a very handy equipment to be included in the list of ambulance equipment. Mr Abu Hassan is also St John Ambulans Malaysia Chief Surgeon, and we are very proud of him. (See foot-note). The immobiliser was invented by him in August, 1996, and was named as Nina Pelvic Immobiliser, after his daughter Sabrina who was born in August, 1990. In a 3 part monograph, he described the indications for early rigid immobilisation of pelvic fracture using the device, its methods of application, and gave its design and the manufacturing technology (1). In an unpublished paper, he reported 20 cases for evaluation in terms of pain relief, haemodynamic status and circulatory effect (blood pressure and pulse rate), changes in pelvic volume, and the reduction of pelvic morphology. More cases are now being studied (personal communication). Syabas to him! He is our local inventor. Besides, I think he is a dynamic Consultant Orthopaedic and Trauma Surgeon.
It is important that a quick and thorough diagnosis as well as therapeutic management according to the special situation and findings is necessary. Effective cooperation of all the different specialists concerned with the management of the patient is mandatory. Massive blood loss immediately after trauma is life-threatening to the patient. To cope with bleeding, all non-invasive measures available should be used. Stable injuries of the pelvis are treated conservatively. In cases of instability, external fixation of the pelvis is mandatory and should be performed as soon as possible. Internal stabilization and osteosynthesis (meaning: surgical fastening of ends of a fractured bone by mechanical means) is another option, bearing in mind the different procedures for the treatment are associated with specific risks and complications.
* Foot-note:
I don’t know how many of you in St. John Ambulance Malaysia are aware that Mr. (Dr) Abu Hassan Asaari Abdullah, a Consultant Traumatologist and Orthopaedic Surgeon and National Consultant to the MOH (Ministry of Health), Malaysia for Emergency Medical and Trauma Services in the country, and the Head of Hospital Kuala Lumpur Emergency Services, is also the Chief Surgeon of St John Ambulans Malaysia. He has invented the Nina Pelvic Immobilizer which he named after his young daughter, Sabrina. With his creative mind, let me take this opportunity to say ‘Syabas’ to this great Malaysian surgeon/inventor of ours. Looking at the fantastic work he has done, from the elaborate Medical Emergency Services set-up at the recent SUKOM Games, to training of First Responders and the Bicycle Medics and Paramedics, to the creation of mobile operating theatres,
Mr. Abu Hassan has literally changed the face of emergency medical services in Malaysia with his innovation and creative mind. Never in the history of Trauma Medicine in Malaysia, has anyone seen someone so visionary and resourceful a person as Mr (Dr) Abu Hassan. He is ambitious, dynamic, and is gifted with visionary ideas on emergency services in Malaysia, and he is on the go all the time. His futuristic vision is the establishment of an Ambulance Service Network for Klang Valley, and eventually nation wide. I hope people in position will support his ideas. I had on a few occasions followed him during his morning ward rounds at the Kuala Lumpur Hospital. One should see him teach during one of his rounds of duty. He is a strict and a good disciplinarian to his staff, a fantastic teacher, and a great surgeon and traumatologist. Not many can teach and explain like him. To add another feature to his cap, he is also an inventor, and he has told me he has invented many other things as well. I take my my hats off to this man. I feel he should get an award for all the work he has done. It will come, but I think his stars are not ripe into position yet. Meantime, we at St John would like to congratulate you a thousand times, Dr. Abu Hassan.
References:
1. Maurer, F. Pelvic Trauma. Aktuelle-Traumatol. (1993 Jul; 23) Suppl 1: 42-9.
2. Abu Hassan, A.A. Early Rigid Immobiliser of Pelvic Fracture using Nina Pelvic Immobilizer. A Monograph, 1998 (Unpublished)
3. Mattox, KL; Bickell W, Pepe; PE. Prospspecting MAST study in 911 patients. J Trauma. (1989), 29:1104.
4. Culllen, DJ; Clyle JP, Teplick R, et al. Cardiovascular pulmonary and renal effects of massively increased intra-abdominal pressure in critically ill patients. Crit Care Med 17:118, 1989.
5. Ganz R, Kroshell RJ, Jakob RP, et al. The anti-shock pelvic clamp. Clin Orthop. (1991), 261:71.
Pelvic Trauma: A Diagnostic
And Therapeutic Challenge
Lim Ju Boo
There was another very short summary statement as a cross reference from some papers (‘papers’ means technical papers from proper journals, and does not mean (news)papers please) I was flipping over last evening, published by Maurer in 1993. He said that it was shown that patients with pelvic trauma often have other multiple injuries that cause special problems (1). Well, I thought about this short, but important statement of his, and I decided that I should write and expand on this subject a little more here.
Crush injuries of the pelvis is commonly seen in about 5% of MVA (motor vehicle accidents) fractures in Malaysia (2). There may be also resultant pelvic fractures from vertical force applied by a fall from a height, the transmission of impact energy anterior-posteriorly, and vice-versa (AP/PA/AP), or laterally from a motor vehicle onto a pedestrian. Injuries to the pelvis can give rise to a number of complications, and they include:
Urogenital:
• Intraperitoneal and extraperitoneal rupture of the bladder
• Rupture of the penis and membranous urethra
Vascular:
• Damage to major vessels
• Massive haemorrhage from retropelvic vascular tear involving the iliac, lumbar, and other smaller arteries (blood loss from 1-4 litres)
• Ecchymosis (bruising and bleeding under the skin) may spread high up into pelvic cavity
• Disemination of intravascular clots
• Consumptive Coagulopathy
Neurological:
• Sciatic nerve damage
• Lumbosacral plexus involvement
Intestinal:
• Paralytic ileus (more common)
• Small intestine, colon and rectum (less common)
Others:
• May also involve extensive tear to the liver, spleen, pancreas, heart, lungs, and great vessels, spinal cord and extremities.
The major cause of mortality and morbidity in pelvic fractures may be due to massive haematoma and blood loss (up to 4 litres) from the damaged retropelvic arteries, especially in pelvic diastasis (diastasis means separation of bones at the epiphysis or joints, not amounting to a fracture), e.g. in ‘open book’ fracture of the pelvis where the symphysis pubis is opened out with appreciable sacro-iliac disruption). In major pelvic fractures where there is extensive bleeding, the chances of the casualty going into hypovolaemic shock are real. In such cases, the priority in first-aid is to immobilize the pelvic bone, and prevent shock (Trendelenburg’s position if necessary). If there are resulting haemorrhage shock, the application of anti-shock garments such as MAST suits. (MAST stands for Military (or Medical) Anti-Shock Trousers) can be one of the initial emergency first-aid treatment (to be done by paramedic or first responder if you like) prior to reduction (reduction is a surgical term to mean restoration to normal position) with external fixateur, and massive blood transfusion in a hospital. However the application of MAST or Pneumatic Antishock Garment (PASG) as advocated by some authorities is not without disadvantages and complications. Surprisingly, it has limited use in hypotensive trauma as shown by Mattox, et al. (3). Although, useful as a splint, by its tamponade effect, but it may also elevate intra-abdominal pressure, and hence may also raise intrathoracic pressure. This would cause resulting in difficulties with ventilation, cardiovascular and renal dysfunction as shown by Cullen, et al (4). In order to overcome the problem, a number of pelvic clamps and devices have been tried to reduce, compress, and immobilize the posterior fragments in a pelvic fracture, thus limiting further movement, tear and bleeding from bone fragments as reported by Ganz et al (5). Moreover, if pelvic fractures involve the long bones as well, there is also the risk of fat emboli (Fat Embolism Syndrome) especially in young adults, in whom fat globules from the long bones of the lower extremities (legs) may enter the lungs causing ARDS (Adult Respiratory Distress Syndrome). However all of these clamps require general anaesthesia for their application which in itself may cause complications in the unstable patient.
One special pelvic clamp device to address the massive bleeding, usually originating from hypogastric arterial involvement, associated with pelvic fractures, was invented by none other than Mr (Dr) Abu Hassan Asaari Abdullah, the Chief Traumatologist and Head of the Department of Emergency Medical and Trauma Services of Kuala Lumpur Hospital. This simple device does not require general anaesthesia for its application, and the application is so simple, it makes it possible for all paramedics, first-responders and first aiders to use it. It is a very handy equipment to be included in the list of ambulance equipment. Mr Abu Hassan is also St John Ambulans Malaysia Chief Surgeon, and we are very proud of him. (See foot-note). The immobiliser was invented by him in August, 1996, and was named as Nina Pelvic Immobiliser, after his daughter Sabrina who was born in August, 1990. In a 3 part monograph, he described the indications for early rigid immobilisation of pelvic fracture using the device, its methods of application, and gave its design and the manufacturing technology (1). In an unpublished paper, he reported 20 cases for evaluation in terms of pain relief, haemodynamic status and circulatory effect (blood pressure and pulse rate), changes in pelvic volume, and the reduction of pelvic morphology. More cases are now being studied (personal communication). Syabas to him! He is our local inventor. Besides, I think he is a dynamic Consultant Orthopaedic and Trauma Surgeon.
It is important that a quick and thorough diagnosis as well as therapeutic management according to the special situation and findings is necessary. Effective cooperation of all the different specialists concerned with the management of the patient is mandatory. Massive blood loss immediately after trauma is life-threatening to the patient. To cope with bleeding, all non-invasive measures available should be used. Stable injuries of the pelvis are treated conservatively. In cases of instability, external fixation of the pelvis is mandatory and should be performed as soon as possible. Internal stabilization and osteosynthesis (meaning: surgical fastening of ends of a fractured bone by mechanical means) is another option, bearing in mind the different procedures for the treatment are associated with specific risks and complications.
* Foot-note:
I don’t know how many of you in St. John Ambulance Malaysia are aware that Mr. (Dr) Abu Hassan Asaari Abdullah, a Consultant Traumatologist and Orthopaedic Surgeon and National Consultant to the MOH (Ministry of Health), Malaysia for Emergency Medical and Trauma Services in the country, and the Head of Hospital Kuala Lumpur Emergency Services, is also the Chief Surgeon of St John Ambulans Malaysia. He has invented the Nina Pelvic Immobilizer which he named after his young daughter, Sabrina. With his creative mind, let me take this opportunity to say ‘Syabas’ to this great Malaysian surgeon/inventor of ours. Looking at the fantastic work he has done, from the elaborate Medical Emergency Services set-up at the recent SUKOM Games, to training of First Responders and the Bicycle Medics and Paramedics, to the creation of mobile operating theatres,
Mr. Abu Hassan has literally changed the face of emergency medical services in Malaysia with his innovation and creative mind. Never in the history of Trauma Medicine in Malaysia, has anyone seen someone so visionary and resourceful a person as Mr (Dr) Abu Hassan. He is ambitious, dynamic, and is gifted with visionary ideas on emergency services in Malaysia, and he is on the go all the time. His futuristic vision is the establishment of an Ambulance Service Network for Klang Valley, and eventually nation wide. I hope people in position will support his ideas. I had on a few occasions followed him during his morning ward rounds at the Kuala Lumpur Hospital. One should see him teach during one of his rounds of duty. He is a strict and a good disciplinarian to his staff, a fantastic teacher, and a great surgeon and traumatologist. Not many can teach and explain like him. To add another feature to his cap, he is also an inventor, and he has told me he has invented many other things as well. I take my my hats off to this man. I feel he should get an award for all the work he has done. It will come, but I think his stars are not ripe into position yet. Meantime, we at St John would like to congratulate you a thousand times, Dr. Abu Hassan.
References:
1. Maurer, F. Pelvic Trauma. Aktuelle-Traumatol. (1993 Jul; 23) Suppl 1: 42-9.
2. Abu Hassan, A.A. Early Rigid Immobiliser of Pelvic Fracture using Nina Pelvic Immobilizer. A Monograph, 1998 (Unpublished)
3. Mattox, KL; Bickell W, Pepe; PE. Prospspecting MAST study in 911 patients. J Trauma. (1989), 29:1104.
4. Culllen, DJ; Clyle JP, Teplick R, et al. Cardiovascular pulmonary and renal effects of massively increased intra-abdominal pressure in critically ill patients. Crit Care Med 17:118, 1989.
5. Ganz R, Kroshell RJ, Jakob RP, et al. The anti-shock pelvic clamp. Clin Orthop. (1991), 261:71.
TRAUMA SYSTEMS IN SHOCK AND RESUSCITATION
Article 5
Lim Ju Boo
Regional Staff Officer for Training
St. John Ambulance Malaysia
The other day, I reviewed some literatures on early care of traumatized patients (1). They cover issues pertaining to the analysis of system function, pre-hospital intravascular volume replacement, diagnosis of proximity vascular injury, the role of emergency thoracotomy (surgical exposure of the thoracic cavity), and the value of transesophageal echocardiography (echogram of the heart, across the chest wall / oesophagus). There were various articles, six of which deal with various aspects of system function, from triage to analysis of outcome. The next series of articles examines the work in progress evaluating optimal fluid resuscitation. Some work on hypertonic saline and dextran combinations has been shown to restore vital signs better than isotonic solutions; they are safe, require smaller volumes, and may improve head injury outcome. Danger lies in the restoration of perfusion without haemorrhage control. There were two articles in the search on emergency thoracotomy that review the indications and outcome in blunt and penetrating trauma. It was demonstrated that survival in blunt trauma is virtually zero. There was also an article and two editorials that summarize the state of art for diagnosis and treatment of proximity (nearest the head and body) vascular injury. Then there are also two articles that describe the potential use of a new technique of transesophageal echocardiography. Unfortunately this new modality has not formed a solid indication at present, and can be considered investigational in trauma care. Hmm! So I have summarized these papers. They are good considerations to ponder on. May I suggest that all doctors, paramedics and those involved in the care of the critically-ill to get hold of the paper.
Reference:
1. Fallom, W.F. Trauma systems, Shock, and Resuscitation. Current Opinion in General Surgery (1993): 40-5.
Lim Ju Boo
Regional Staff Officer for Training
St. John Ambulance Malaysia
The other day, I reviewed some literatures on early care of traumatized patients (1). They cover issues pertaining to the analysis of system function, pre-hospital intravascular volume replacement, diagnosis of proximity vascular injury, the role of emergency thoracotomy (surgical exposure of the thoracic cavity), and the value of transesophageal echocardiography (echogram of the heart, across the chest wall / oesophagus). There were various articles, six of which deal with various aspects of system function, from triage to analysis of outcome. The next series of articles examines the work in progress evaluating optimal fluid resuscitation. Some work on hypertonic saline and dextran combinations has been shown to restore vital signs better than isotonic solutions; they are safe, require smaller volumes, and may improve head injury outcome. Danger lies in the restoration of perfusion without haemorrhage control. There were two articles in the search on emergency thoracotomy that review the indications and outcome in blunt and penetrating trauma. It was demonstrated that survival in blunt trauma is virtually zero. There was also an article and two editorials that summarize the state of art for diagnosis and treatment of proximity (nearest the head and body) vascular injury. Then there are also two articles that describe the potential use of a new technique of transesophageal echocardiography. Unfortunately this new modality has not formed a solid indication at present, and can be considered investigational in trauma care. Hmm! So I have summarized these papers. They are good considerations to ponder on. May I suggest that all doctors, paramedics and those involved in the care of the critically-ill to get hold of the paper.
Reference:
1. Fallom, W.F. Trauma systems, Shock, and Resuscitation. Current Opinion in General Surgery (1993): 40-5.
Article 4
Acid-Base Response to High
Volume Haemofiltration in the Critically Ill
Lim Ju Boo
The effects of acid-base balance on the body buffers, lung function and kidney function are well established. Disturbances in the acid-base balance may be featured by mild CNS (central nervous system) dysfunction and abnormalities of respiration. Acidosis may be suggested by a marked decline in conscious level with confusion and irritability. A classical sign is Kussmaul’s respiration (deep, sighing breathing). Clinical signs are rare in alkalosis (blood pH shifted towards alkalinity), but severe alkalosis may be accompanied by depression of conscious level and hypoventilation. Tetany (muscle spasms due to muscular hyperexcitability) may be present due to low ionised calcium.
The acid-base and cardiorespiratory effects of intermittently pumped high-volume veno-venous haemofiltration (HVHF) using replacement fluid containing lactate as the source of biocarbonate in critically ill-patient was studied (haemofiltration is a form of haemodialysis which requires the same access to the blood circulation as haemodialysis. The patient’s cardiac output drives the blood through a small, highly permeable filter: this permits the isolation of fluid and solutes: this haemofiltrate is measured, discarded, and is replaced with an isotonic solution).
It was demonstrated that there was a significant hyperlactataemia (too much of lactic acid in the blood) throughout the procedure, but there was no deterioration in acid-base status, haemodynamics (the forces involved in circulating blood round the body), or oxygen delivery. These observations suggest that the worsening of acidosis and hypotension that have been described with this technique can be avoided by appropriate monitoring and resuscitation prior to haemofiltration, and may be due to unrecognized inadequacies in the oxygen transport system as shown by Nimmo (1). It is known that in critically ill patients with inadequate ventilation, and hypoperfusion, there will be shift in normal cellular energy transfer from aerobic to anarobic metabolism, resulting in metabolic acidosis. The relationship between elevated serum lactic acid and hypovolemic shock and even death is well known, as shown long ago by Huchabee (2), and more lately by Weil, et al (3).
Reference:
1. Nimmo, G.R; Mackenzie, S.J; Walker, S; Nicol, M; Grant, I.S. Nephrol-Dial-Transplant. 1993; 8(9): 854-7.
2 Huckabee W. Relationships of pyruvate and lactate during anaerobic metabolism: Effects of infusion of pyruvate or glucose and of hyperventilation. J Clin Invest (1958) 37:244
3 Weil M, Afifi A. Experimental and clinical studies on lactate and pyruvate as indication of the severity of acute circulatory failure. Circulation (1990), 41:989
Acid-Base Response to High
Volume Haemofiltration in the Critically Ill
Lim Ju Boo
The effects of acid-base balance on the body buffers, lung function and kidney function are well established. Disturbances in the acid-base balance may be featured by mild CNS (central nervous system) dysfunction and abnormalities of respiration. Acidosis may be suggested by a marked decline in conscious level with confusion and irritability. A classical sign is Kussmaul’s respiration (deep, sighing breathing). Clinical signs are rare in alkalosis (blood pH shifted towards alkalinity), but severe alkalosis may be accompanied by depression of conscious level and hypoventilation. Tetany (muscle spasms due to muscular hyperexcitability) may be present due to low ionised calcium.
The acid-base and cardiorespiratory effects of intermittently pumped high-volume veno-venous haemofiltration (HVHF) using replacement fluid containing lactate as the source of biocarbonate in critically ill-patient was studied (haemofiltration is a form of haemodialysis which requires the same access to the blood circulation as haemodialysis. The patient’s cardiac output drives the blood through a small, highly permeable filter: this permits the isolation of fluid and solutes: this haemofiltrate is measured, discarded, and is replaced with an isotonic solution).
It was demonstrated that there was a significant hyperlactataemia (too much of lactic acid in the blood) throughout the procedure, but there was no deterioration in acid-base status, haemodynamics (the forces involved in circulating blood round the body), or oxygen delivery. These observations suggest that the worsening of acidosis and hypotension that have been described with this technique can be avoided by appropriate monitoring and resuscitation prior to haemofiltration, and may be due to unrecognized inadequacies in the oxygen transport system as shown by Nimmo (1). It is known that in critically ill patients with inadequate ventilation, and hypoperfusion, there will be shift in normal cellular energy transfer from aerobic to anarobic metabolism, resulting in metabolic acidosis. The relationship between elevated serum lactic acid and hypovolemic shock and even death is well known, as shown long ago by Huchabee (2), and more lately by Weil, et al (3).
Reference:
1. Nimmo, G.R; Mackenzie, S.J; Walker, S; Nicol, M; Grant, I.S. Nephrol-Dial-Transplant. 1993; 8(9): 854-7.
2 Huckabee W. Relationships of pyruvate and lactate during anaerobic metabolism: Effects of infusion of pyruvate or glucose and of hyperventilation. J Clin Invest (1958) 37:244
3 Weil M, Afifi A. Experimental and clinical studies on lactate and pyruvate as indication of the severity of acute circulatory failure. Circulation (1990), 41:989
CAN WE GET POISONING BY DRINKING ALCOHOL OR VINEGAR?
Article 3
(Just for Academic Stimulation and Fun Reading only)
Lim Ju Boo
The article below was written after a light academic reflection. It has little to do with first-aid.
It was written just for interest, and for argument sake only. It is just a brain-storming session within me. I am sure some drinkers don’t agree with me.
As a hind thought after writing the previous article, cause me to wonder whether some itchy readers may ask me whether or not after the jellyfish venom has entered the body, can the victim drink a lot of whisky, brandy, wine and toddy (as an excuse for drinking) and vinegar to combat the venom since the BAA first aid manual prescribed applying alcohol or vinegar.
If a small quantity of drinkable alcohol (ethanol) from say whisky, brandy, wine, toddy, fermented beverages, beer and stout is drunk, nothing happens. The body is capable of dealing with it. Alcohol is like a nutrient. It is easily burnt off and supplies the calories like any other energy-giving food substances. At the most, people may show up a little tipsy, a little more talkative and boisterous. We can easily see this effect gradually building up, say in the case of our colleagues in St John Ambulance Malaysia, Regional Superintendent Lee Wing Kwong and the then Regional Secretary (now Regional Superintendent) Michael Yeow Kiew Meng who sat at the same table as myself during a dinner at Shah Alam Club on the 28th November in honour of Dato’ Dr. Low Bon Tick. I could see that once a while they really enjoyed themselves harmlessly. Very soon their enjoyment and merriment spread to the adjourning table where other officers were just as high and boisterous. While this was going on, others would react differently. They suddenly become very quiet, but very flashed-up on the face (due to vaso-dilation). This was the case with ADO Lim Kian Tong who became an ‘instant mat salleh’ on the face even after one sip of beer. The effect of alcohol on me is nausea. The effects of alcohol may delay the reflexes, and the response time lengthened. In severe alcohol intoxication, besides inebriation, we will be presented with ataxia (defective muscular control), blurred vision, tachycardia (increased heart rate of > 100 b/m), impaired level of conciousness (stupor), including coma, severe hypoglycaemia (low blood sugar), convulsions, slow respiration and possibly death. We will never be able to reach a level of alcohol concentration in the blood sufficient to denature jellyfish toxin. It would probably dehydrate and denature the protein make-up of our tissues first ? That is why alcohol can be used as a preservative for preserving the carcasses of small animals kept in the laboratory. At low very low levels, the alcohol is easily burnt off with the help of a liver enzyme – alcohol oxidoreductase (formerly called alcohol dehydrogenase). It will require an alcohol concentration of at least 75% to denature any soluble protein, say in a serum or venom. Well, before the blood concentration can reach that level, you might have to be treated for alcohol poisoning instead of for jellyfish poisoning. That’s the effect of short-term ‘alcoholism’ or rather acute alcohol intoxication. But if you are a chronic drinker, anything can happen even if you take small quantities each time over many years. There are a number of alcohol-related disorders (pathological intoxication) you may choose from; anything from delirium tremens, alcoholic hepatitis, alcoholic cirrhosis, hepatocellular carcinoma, cardiomyopathies (diseases of the heart muscles), hypophosphataemia (low blood phosphate level), down the long list, to thiamin deficiency and Wernicke’ encephalopathy (a neurological disorder associated with chronic alcoholism). This condition coexists with another condition ‘Korsakoff syndrome’ and Korsakoff psychosis which are also associated with alcoholism and nutritional (thiamin) deficiency. I am not going down the list any further. This list is frightening enough. The chose is ours. Either way, don’t drink, nor try to treat jellyfish sting by drinking. First-aid books do not prescribe alcohol for drinking. It’s only for external application.
We may ask what about drinking vinegar then? Like alcohol, vinegar may also be considered a food item. Unfortunately, the ‘vinegar’ we buy these days is actually diluted synthetic acetic acid made from acetaldehyde by oxidation. Acetaldehyde solution, or formalin, is a preservative use for embalming a dead body. Sorry about that, because they don’t make the natural traditional vinegar from flour, tapioca, rice, and wine by fermenting the alcohol produced with bacteria anymore. Anything we put into our mouths these days seems man-made in the factory, including synthetic 'shark‘s fins' I had at a hotel yesterday. Taken in small quantities, vinegar, as we all do when we add it to shark’s fin soup, or any food preparation does us no harm. Vinegar, is a mild organic acid, and is easily handled by the body. It enters the Kreb Cycle (a circular metabolic pathway, also called citric acid cycle, which is the power house of the body) as an intermediary metabolite (acetate), and gets burned off by a process called oxidative phosphorylation without a trace. However, if very large quantities of vinegar or mild consumable acids are taken, it will upset a homeostatic mechanism called the acid-base balance (the buffering system) of the body. The acid-base control involves body buffers, lung function, and kidney function (in order of speed of response). The biochemistry and physiology of this balance is a very lengthy and complicated subject, but in a very brief way, all we can say is that all acids add hydrogen ions (H +) to the body. This is regulated by both kidneys and lungs as shown by the equations: H+ + HCO- 3 = H2O + CO2. The HCO- 3 is regulated by the kidneys, and the CO2, regulated by the lungs. If hydrogen ions (H +) is added to the blood, e.g. poisoning by an acid, this will give rise to a condition called ‘metabolic acidosis’, and the equation is pushed to the right. Respiration rate will increase (hyperventilation) to metabolically ‘blow off’ the excess CO2, giving rise to Kussmaul’s respiration (laboured, deep breathing), similar to one of the features of serve, uncontrolled diabetes. This is because the excess CO 2 (carbon dioxide) will trigger off chemoreceptors (small carotid bodies that can respond to changes in chemical substances in the body) lodged to a twig of a small branch of the external carotid artery close to the carotid sinus. Other chemosensitive areas responding to pH changes in the arterial blood are located very near the surface of the medulla near the point of entry of the glossopharyngeal and vagus nerves (9th and 10th cranial nerves respectively). It also involves the aortic bodies, located near the arch of the aorta, where stretch receptors (baroreceptors) that control blood pressure are also located. Carbon dioxide is a very powerful stimulus to ventilation; an increase in arterial blood paCO2 (partial pressure of CO2) of 2 to 3 mm Hg causes the rate of ventilation to double. If the CO2 continues to rise, the equation is pushed to the left, increasing the [H +] in the blood (respiratory acidosis). Electrolyte and acid-base balance is very complex and lengthy subject, and hyper or hypo conditions of acidosis and alkalosis give rise to various responses, anything from arrythmias (abnormal heart-beat, e.g. from hyperkalaemia - too much of serum potassium) to tetany (muscular cramps and spasms from low serum calcium or to alkalosis). Latent tetany is best recognised by eliciting the Trousseau’s manoeuvre – carpopedal spasm, or ‘obstetrician’s hand’, to confusional states, linked to various disease conditions. The understanding of acid-base balance, as well as electrolyte balance occupies full and very large chapters in almost all advanced textbooks of physiology, biochemistry, nutrition and medicine. We will of course not go into them. Suffice to say that their understanding has a good deal of applications in the care of critically ill patients, and I shall write a very brief example on this separately in a review paper later. (See article on “Acid-base responses to high-volume haemofiltration in the critically ill). However if you drink concentrated ‘vinegar’ which is glacial acetic acid, then the scenario is going to be entirely different. You will get acid burns on your mouth, throat, esophagus, stomach, and perhaps the small intestines. It will burn right through. We will have to immediately apply first-aid for corrosive substances for your GI (gastrointestinal) tract instead of treatment for jellyfish sting? So neither drinking alcohol nor vinegar is going to work. That’s not the way to do things. We will have to look for proper anti-venom. Whether or not vanilla taken in orally is going to work, is an interesting question. We (or at least myself) would sure like to examine carefully the data and findings of the University of Malaya medical team. This will have a bearing on the practice of first-aid which needs to be constantly updated through continuous research and education. In the meantime, I am very tempted to have a vanilla ice-cream with or without the jelly (fish). I am going out to buy one now. I will be right back to continue with more stories. Anyone care to join me?
(Just for Academic Stimulation and Fun Reading only)
Lim Ju Boo
The article below was written after a light academic reflection. It has little to do with first-aid.
It was written just for interest, and for argument sake only. It is just a brain-storming session within me. I am sure some drinkers don’t agree with me.
As a hind thought after writing the previous article, cause me to wonder whether some itchy readers may ask me whether or not after the jellyfish venom has entered the body, can the victim drink a lot of whisky, brandy, wine and toddy (as an excuse for drinking) and vinegar to combat the venom since the BAA first aid manual prescribed applying alcohol or vinegar.
If a small quantity of drinkable alcohol (ethanol) from say whisky, brandy, wine, toddy, fermented beverages, beer and stout is drunk, nothing happens. The body is capable of dealing with it. Alcohol is like a nutrient. It is easily burnt off and supplies the calories like any other energy-giving food substances. At the most, people may show up a little tipsy, a little more talkative and boisterous. We can easily see this effect gradually building up, say in the case of our colleagues in St John Ambulance Malaysia, Regional Superintendent Lee Wing Kwong and the then Regional Secretary (now Regional Superintendent) Michael Yeow Kiew Meng who sat at the same table as myself during a dinner at Shah Alam Club on the 28th November in honour of Dato’ Dr. Low Bon Tick. I could see that once a while they really enjoyed themselves harmlessly. Very soon their enjoyment and merriment spread to the adjourning table where other officers were just as high and boisterous. While this was going on, others would react differently. They suddenly become very quiet, but very flashed-up on the face (due to vaso-dilation). This was the case with ADO Lim Kian Tong who became an ‘instant mat salleh’ on the face even after one sip of beer. The effect of alcohol on me is nausea. The effects of alcohol may delay the reflexes, and the response time lengthened. In severe alcohol intoxication, besides inebriation, we will be presented with ataxia (defective muscular control), blurred vision, tachycardia (increased heart rate of > 100 b/m), impaired level of conciousness (stupor), including coma, severe hypoglycaemia (low blood sugar), convulsions, slow respiration and possibly death. We will never be able to reach a level of alcohol concentration in the blood sufficient to denature jellyfish toxin. It would probably dehydrate and denature the protein make-up of our tissues first ? That is why alcohol can be used as a preservative for preserving the carcasses of small animals kept in the laboratory. At low very low levels, the alcohol is easily burnt off with the help of a liver enzyme – alcohol oxidoreductase (formerly called alcohol dehydrogenase). It will require an alcohol concentration of at least 75% to denature any soluble protein, say in a serum or venom. Well, before the blood concentration can reach that level, you might have to be treated for alcohol poisoning instead of for jellyfish poisoning. That’s the effect of short-term ‘alcoholism’ or rather acute alcohol intoxication. But if you are a chronic drinker, anything can happen even if you take small quantities each time over many years. There are a number of alcohol-related disorders (pathological intoxication) you may choose from; anything from delirium tremens, alcoholic hepatitis, alcoholic cirrhosis, hepatocellular carcinoma, cardiomyopathies (diseases of the heart muscles), hypophosphataemia (low blood phosphate level), down the long list, to thiamin deficiency and Wernicke’ encephalopathy (a neurological disorder associated with chronic alcoholism). This condition coexists with another condition ‘Korsakoff syndrome’ and Korsakoff psychosis which are also associated with alcoholism and nutritional (thiamin) deficiency. I am not going down the list any further. This list is frightening enough. The chose is ours. Either way, don’t drink, nor try to treat jellyfish sting by drinking. First-aid books do not prescribe alcohol for drinking. It’s only for external application.
We may ask what about drinking vinegar then? Like alcohol, vinegar may also be considered a food item. Unfortunately, the ‘vinegar’ we buy these days is actually diluted synthetic acetic acid made from acetaldehyde by oxidation. Acetaldehyde solution, or formalin, is a preservative use for embalming a dead body. Sorry about that, because they don’t make the natural traditional vinegar from flour, tapioca, rice, and wine by fermenting the alcohol produced with bacteria anymore. Anything we put into our mouths these days seems man-made in the factory, including synthetic 'shark‘s fins' I had at a hotel yesterday. Taken in small quantities, vinegar, as we all do when we add it to shark’s fin soup, or any food preparation does us no harm. Vinegar, is a mild organic acid, and is easily handled by the body. It enters the Kreb Cycle (a circular metabolic pathway, also called citric acid cycle, which is the power house of the body) as an intermediary metabolite (acetate), and gets burned off by a process called oxidative phosphorylation without a trace. However, if very large quantities of vinegar or mild consumable acids are taken, it will upset a homeostatic mechanism called the acid-base balance (the buffering system) of the body. The acid-base control involves body buffers, lung function, and kidney function (in order of speed of response). The biochemistry and physiology of this balance is a very lengthy and complicated subject, but in a very brief way, all we can say is that all acids add hydrogen ions (H +) to the body. This is regulated by both kidneys and lungs as shown by the equations: H+ + HCO- 3 = H2O + CO2. The HCO- 3 is regulated by the kidneys, and the CO2, regulated by the lungs. If hydrogen ions (H +) is added to the blood, e.g. poisoning by an acid, this will give rise to a condition called ‘metabolic acidosis’, and the equation is pushed to the right. Respiration rate will increase (hyperventilation) to metabolically ‘blow off’ the excess CO2, giving rise to Kussmaul’s respiration (laboured, deep breathing), similar to one of the features of serve, uncontrolled diabetes. This is because the excess CO 2 (carbon dioxide) will trigger off chemoreceptors (small carotid bodies that can respond to changes in chemical substances in the body) lodged to a twig of a small branch of the external carotid artery close to the carotid sinus. Other chemosensitive areas responding to pH changes in the arterial blood are located very near the surface of the medulla near the point of entry of the glossopharyngeal and vagus nerves (9th and 10th cranial nerves respectively). It also involves the aortic bodies, located near the arch of the aorta, where stretch receptors (baroreceptors) that control blood pressure are also located. Carbon dioxide is a very powerful stimulus to ventilation; an increase in arterial blood paCO2 (partial pressure of CO2) of 2 to 3 mm Hg causes the rate of ventilation to double. If the CO2 continues to rise, the equation is pushed to the left, increasing the [H +] in the blood (respiratory acidosis). Electrolyte and acid-base balance is very complex and lengthy subject, and hyper or hypo conditions of acidosis and alkalosis give rise to various responses, anything from arrythmias (abnormal heart-beat, e.g. from hyperkalaemia - too much of serum potassium) to tetany (muscular cramps and spasms from low serum calcium or to alkalosis). Latent tetany is best recognised by eliciting the Trousseau’s manoeuvre – carpopedal spasm, or ‘obstetrician’s hand’, to confusional states, linked to various disease conditions. The understanding of acid-base balance, as well as electrolyte balance occupies full and very large chapters in almost all advanced textbooks of physiology, biochemistry, nutrition and medicine. We will of course not go into them. Suffice to say that their understanding has a good deal of applications in the care of critically ill patients, and I shall write a very brief example on this separately in a review paper later. (See article on “Acid-base responses to high-volume haemofiltration in the critically ill). However if you drink concentrated ‘vinegar’ which is glacial acetic acid, then the scenario is going to be entirely different. You will get acid burns on your mouth, throat, esophagus, stomach, and perhaps the small intestines. It will burn right through. We will have to immediately apply first-aid for corrosive substances for your GI (gastrointestinal) tract instead of treatment for jellyfish sting? So neither drinking alcohol nor vinegar is going to work. That’s not the way to do things. We will have to look for proper anti-venom. Whether or not vanilla taken in orally is going to work, is an interesting question. We (or at least myself) would sure like to examine carefully the data and findings of the University of Malaya medical team. This will have a bearing on the practice of first-aid which needs to be constantly updated through continuous research and education. In the meantime, I am very tempted to have a vanilla ice-cream with or without the jelly (fish). I am going out to buy one now. I will be right back to continue with more stories. Anyone care to join me?
Saturday, April 24, 2010
First Aid Management of Anaphylaxis & Anaphylactic Shock
Article 2
Management of Anaphylaxis &
Anaphylactic Shock
Lim Ju Boo
Regional Staff Officer for Training
St John Ambulance Malaysia
Anaphylactic shock, is a shock resulting from a very severe allergic reaction when the body is challenged with an antigen in which the body had previously being sensitized (e.g. intake of certain foods like peanuts, beef, prawns, or contact with certain plants, latex, horse serum, an insect bite, venom, antivenin, antibiotics, especially penicillin and antitetanus injections, etc.). However, I must admit that food taken orally rarely result in anaphylactic shock, except for allergic reactions to those who are sensitive. A severe hypersensitive state (syn. Serum sickness) is called anaphylaxis. It is the result of an antigen-antibody reaction when the body had previously been challenged by an antigen. Initially there may be no reaction. Severe reactions occur on second and subsequent exposures when antibodies (chiefly the immunoglobulins called IgE) begin to build up to trigger off wide spread histamine release by mast cells. Severe allergic reactions, short of anaphylactic shock, may also occur if; say a baby takes an egg or cow’s milk, or foods for which he is sensitive.
No pre-exposure:
A baby may not have been previously exposed to eggs or cow’s protein, but his mother was, and the specific antibodies (IgE) from the maternal blood had already entered his foetal circulation during intra-uterine life. Similarly, a patient developing anaphylactic shock from a single, first-time penicillin injection may have already been sensitized previously by moulds (Penicillium notatum, P. chrysogenumin) in the food and air even in exceedingly minute amounts (1). Anaphylaxis is normally characterized by extensive angiooedema (a very severe form of urticaria and swelling) to the laryngeal region, and there may be bronchial spasm. This may lead to respiratory and circulatory collapse. Death can occur within minutes when the body is challenged with a serum, venom or any allergen for which the person is highly sensitive to. The victim must be transported to a hospital immediately where adrenaline, steroids, antihistamine drugs, and oxygen may be administered.
First line of management:
There may be no first-aid for this condition, except to help the victim to breathe better, treat for shock and prepare for resuscitation if necessary. However as it involves bronchospasm, before cardiopulmonary collapse set in, it may be helpful if enquiries are made from bystanders who may be milling around, to find out if any of them is an asthmatic, and who may happen to carry a salbutamol (a bronchodilator) inhaler. Interesting questions we would ask here are: (i) Would one or two puff from such an inhaler borrowed from an asthmatic who may happen to be nearby, be of help to ease or reverse the bronchospasm while waiting for an ambulance to arrive or when the situation is getting very critical, and there is going to be a delay in transporting the patient? (ii) Can a first-aider borrow someone’s inhaler in an emergency when acute bronchospasms and death becomes inevitable? Is it allowed or ethical? (iii) Would such interim measure be helpful?
Alternative approach:
For that matter, even a common cough syrup - diphenhydramine hydrocloride (Benadryl) is also known to do the trick of counteracting excessive and extensive histamine release. In a hospital setting, diphenhydramine HCl (not the syrup) is given i.v. (intravenously) at a dose of 20 mg slowly, or 1-2 mg/kg up to 50 mg i.m (intramuscularly) over 3 mintues (2, 3, 4, 5). The equivalent dose is just 2 teaspoonful of the syrup per kilogram of body weight. Again the question we will have to ask is whether or not a remedy as simple as a cough syrup can save a life in such a crisis, albeit the medication in the form of a syrup taken orally is very mild, as it is not as rapidly absorbed and fast-acting as it would have been, if given parenterally, say via vascular access (intravenously). You may think that this rationale is correct, but I do not know the answer myself. Unless a study is done, I don’t think anyone can answer for certain. We may think otherwise, but sometimes unexpected results suddenly show up in clinical research. Somebody must carry out a study.
The golden hour:
Like in AMI, the first hour determines the chances of survival. In first-aid of asthma, or shock nothing much can be offered other than sitting the victim up or in a comfortable position to ease breathing. If there is shock, treat for shock (Trendelenburg position), and prepare to resuscitate if necessary, before sending the victim to a hospital. But what should first reponders / first-aiders do in an extreme crisis, when life or death is just minutes away, and transport is going to be delayed, or an ambulance being caught in a traffic jam on the way to a hospital? Should emergency medication be given by a first-aider if he is properly trained? These are questions people should be asking? I know that in the United States, Emergency Medical Technician-Basic (someone whose training is even less than that of a paramedics) are allowed to give even epinephrine (adrenaline) injections via an auto-injector to an anaphylactic victim, whereas paramedics are trained for even invasive procedures like insertion of endotracheal tubes, initiation of IV lines, administration of medications, interpretation of electrocardiograms, and cardiac defibrillations.
So are paramedics in Australia, France, and some other countries trained for this (8). I read that when Princess Diana was injured in the Paris car crash, ambulance crew called to the scene, had to stop the ambulance on the way to the hospital so that the ambulance crew could administer intracardiac adrenaline to her, although this procedure is now debatable, and no more recommended by the United Kingdom Resuscitation Council. Shouldn’t first-aiders/first responders, paramedics, ambulance crew etc. in this country be similarly trained up to that standard as well?
Alternative first aid medicine:
Interestingly, in one form of alternative medicine (reflexology), the modality of treatment is to massage certain pressure zones on the soles of both feet. This seems to elicit a response by sending pulses to the brain, which in turn stimulates the sympathetic autonomic nervous system* (see foot-note for explanation) to force the bronchi to relax, simultaneously sending another set of impulses to the adrenal glands (lies superior to the kidneys) to excite the cortex (outer layer) of this gland to release all the corticosteroidal hormones, and also the medulla (inner layer) of the adrenal gland to discharge the much needed adrenaline and noradrenaline into the blood. Noradrenaline is also produced by the sympathetic ganglia other than from the medulla. These natural hormones produced by the body are exactly the same drugs (other than antihistamines) a doctor would have injected to counteract the anaphylaxis. I know of at least two cases where patients recovered (at least for bronchial asthma) uneventfully through this procedure without any further intervention. This drug-free approach seems very interesting. However a larger population study would be needed for statistical analysis on this harmless modality if conventional first-aid becomes ineffective in certain situations.
Coffee as a bronchodilator:
Let us now move on to consider another very safe and common bronchodilator. And that’s just plain black coffee. Numerous clinical studies and I shall quote just two (6, 7), have shown that coffee has the same therapeutic value as aminophylline, a bronchodilating agent. Aminophylline is given at a dose of 250-350 mg i.v. over 15 minutes to keep the bronchioles patent in asthmatic patients (3). This dose is equivalent to 600 mg of caffeine which is found in two cups of very strong black coffee (no milk please. Cow’s milk protein can trigger off an allergic reaction, and makes the problem worse). Coffee contains these two drugs – aminophylline and theophylline, already present naturally in it. Both these agents are used as powerful bronchodialators in prolonged and severe asthma (status asthmaticus). Even if the aminophylline and theophylline are removed from coffee, the caffeine in the coffee itself will metabolically breakdown into these two natural drugs and make them available to the body.
Alternatives with similar mode of action:
Consider these mechanisms as some of the possibilities in first-aid for bronchospasm and angiooedema as features of anaphylaxis? I do not know the answers with certainty myself, but I am thinking of them as possibilities in the light of our scientific knowledge, and the work done by others (3,6,7). Again, questions we must seriously ask are: Can some of these harmless naturally occurring substances which show similar and promising pharmacological actions as the more powerful drugs, be used in the interim before medical intervention with more powerful and faster acting agents becomes accessible to the victim? Can they be given in the first place? Should they be given? Will they be effective? Of course one must remember not to feed anything through the mouth, not even a teaspoonful of water (except wetting the lips with water) if the patient is unconscious or unable to swallow. Once in the hospital, all medication or fluid may have to be given parenterally (non-oral route) via vascular access. For the moment the priority for the first-aider is merely to secure the airway, ensure breathing, and circulation, and transport the victim as early as possible to a hospital. Good luck. Hope you wont meet such a casualty. It can be very eventful.
Foot-note:
By the way, for those not familiar with the meaning of autonomic nervous system, very briefly, the autonomic nervous system is part of the central nervous system, and is made up of ganglia and fibres. It is divided into two major components – the sympathetic and the parasympathetic nervous systems. The functions of both systems are to control involuntary activities involving the smooth muscles, such as those responsible for respiration, heart beat, digestion, pupil size, etc. The sympathetic and parasympathetic nervous systems work in opposite action to one another. One stimulates, and the other inhibits the action.
Physiology of the 10th cranial nerve:
For example, the sympathetic nerve accelerates the heart beat, while the parasympathetic slows it down. The 10th cranial nerve is the vagus nerve, and is a parasympathetic nerve that controls and slows down the heart-rate. The nerve that accelerates the heart is called the accelerator or augmentor sympathetic nerve. If the vagus nerve is stimulated, it will slow down the heart rate to the extent of inducing a cardiac arrest (similar to giving excessive potassium). But if the stimulus is continuously applied, the heart will escape this vagal restraint, and commence to beat again (‘vagal escape of the heart’), with the first few ventricular contractions being exceptionally forceful. I must say nature is very kind to us to ensure we continue to survive.
Vagal escape:
If the vagus nerve is cut, or temporary paralyzed by a full dose of atropine (a drug with parasympatholytic action), the heart rate will be doubled (150 –180 beats per minute). Just for information sake, the vagus nerve is not there just to control the heart. After it emerges from the medulla oblongata (part of the brain stem), this longest cranial nerve starts to supply branches to the larynx, pharynx, trachea, heart, lungs, and most of the digestive system, and controls all of them.
References:
1. Yadav, M., Formerly, Professor of Immunology, University of Malaya, currently Consultant Immunologist and Allergist. Penicillin and Anaphylaxis. A Personal Communication. Nov. 1998.
2. Feng, P.H., Fock, K.M., Eng, Philip. Handbook of Acute Medicine (5th edition, 1992), Pages 76-78. APAC Publishers, Singapore.
3. Robinson, R., Stott, Robin. Medical Emergencies, Diagnosis and Management (6th edition, 1994), 345-346. CBS Publishers & Distributors, Delhi, India
4. Bochner B. et al. (1991). Anaphylaxis. N. Engl. J. Med. 324:1785.
5. Brueton M. et al. (1991). Management of anaphylaxis. Hospital Update May, page 386.
6. Becker, A.B., et al. The Bronchodilator Effects and Pharmacokinetics of Caffeine in Asthma.” New Engl. J. Med. (March 22, 1984). 310 (12): 743-746.
7. Gong. H., Jr., et al. Bronchodilator Effects of Caffeine in Coffee. A Dose-Response Study of Asthmatic Subjects.” Chest (March, 1986), 89(3): 335-342.
8. Brady Emergency Care, Grant, H.D, et al. (7th edition, 1995). Prentice-Hall International (UK) Ltd. London.
Management of Anaphylaxis &
Anaphylactic Shock
Lim Ju Boo
Regional Staff Officer for Training
St John Ambulance Malaysia
Anaphylactic shock, is a shock resulting from a very severe allergic reaction when the body is challenged with an antigen in which the body had previously being sensitized (e.g. intake of certain foods like peanuts, beef, prawns, or contact with certain plants, latex, horse serum, an insect bite, venom, antivenin, antibiotics, especially penicillin and antitetanus injections, etc.). However, I must admit that food taken orally rarely result in anaphylactic shock, except for allergic reactions to those who are sensitive. A severe hypersensitive state (syn. Serum sickness) is called anaphylaxis. It is the result of an antigen-antibody reaction when the body had previously been challenged by an antigen. Initially there may be no reaction. Severe reactions occur on second and subsequent exposures when antibodies (chiefly the immunoglobulins called IgE) begin to build up to trigger off wide spread histamine release by mast cells. Severe allergic reactions, short of anaphylactic shock, may also occur if; say a baby takes an egg or cow’s milk, or foods for which he is sensitive.
No pre-exposure:
A baby may not have been previously exposed to eggs or cow’s protein, but his mother was, and the specific antibodies (IgE) from the maternal blood had already entered his foetal circulation during intra-uterine life. Similarly, a patient developing anaphylactic shock from a single, first-time penicillin injection may have already been sensitized previously by moulds (Penicillium notatum, P. chrysogenumin) in the food and air even in exceedingly minute amounts (1). Anaphylaxis is normally characterized by extensive angiooedema (a very severe form of urticaria and swelling) to the laryngeal region, and there may be bronchial spasm. This may lead to respiratory and circulatory collapse. Death can occur within minutes when the body is challenged with a serum, venom or any allergen for which the person is highly sensitive to. The victim must be transported to a hospital immediately where adrenaline, steroids, antihistamine drugs, and oxygen may be administered.
First line of management:
There may be no first-aid for this condition, except to help the victim to breathe better, treat for shock and prepare for resuscitation if necessary. However as it involves bronchospasm, before cardiopulmonary collapse set in, it may be helpful if enquiries are made from bystanders who may be milling around, to find out if any of them is an asthmatic, and who may happen to carry a salbutamol (a bronchodilator) inhaler. Interesting questions we would ask here are: (i) Would one or two puff from such an inhaler borrowed from an asthmatic who may happen to be nearby, be of help to ease or reverse the bronchospasm while waiting for an ambulance to arrive or when the situation is getting very critical, and there is going to be a delay in transporting the patient? (ii) Can a first-aider borrow someone’s inhaler in an emergency when acute bronchospasms and death becomes inevitable? Is it allowed or ethical? (iii) Would such interim measure be helpful?
Alternative approach:
For that matter, even a common cough syrup - diphenhydramine hydrocloride (Benadryl) is also known to do the trick of counteracting excessive and extensive histamine release. In a hospital setting, diphenhydramine HCl (not the syrup) is given i.v. (intravenously) at a dose of 20 mg slowly, or 1-2 mg/kg up to 50 mg i.m (intramuscularly) over 3 mintues (2, 3, 4, 5). The equivalent dose is just 2 teaspoonful of the syrup per kilogram of body weight. Again the question we will have to ask is whether or not a remedy as simple as a cough syrup can save a life in such a crisis, albeit the medication in the form of a syrup taken orally is very mild, as it is not as rapidly absorbed and fast-acting as it would have been, if given parenterally, say via vascular access (intravenously). You may think that this rationale is correct, but I do not know the answer myself. Unless a study is done, I don’t think anyone can answer for certain. We may think otherwise, but sometimes unexpected results suddenly show up in clinical research. Somebody must carry out a study.
The golden hour:
Like in AMI, the first hour determines the chances of survival. In first-aid of asthma, or shock nothing much can be offered other than sitting the victim up or in a comfortable position to ease breathing. If there is shock, treat for shock (Trendelenburg position), and prepare to resuscitate if necessary, before sending the victim to a hospital. But what should first reponders / first-aiders do in an extreme crisis, when life or death is just minutes away, and transport is going to be delayed, or an ambulance being caught in a traffic jam on the way to a hospital? Should emergency medication be given by a first-aider if he is properly trained? These are questions people should be asking? I know that in the United States, Emergency Medical Technician-Basic (someone whose training is even less than that of a paramedics) are allowed to give even epinephrine (adrenaline) injections via an auto-injector to an anaphylactic victim, whereas paramedics are trained for even invasive procedures like insertion of endotracheal tubes, initiation of IV lines, administration of medications, interpretation of electrocardiograms, and cardiac defibrillations.
So are paramedics in Australia, France, and some other countries trained for this (8). I read that when Princess Diana was injured in the Paris car crash, ambulance crew called to the scene, had to stop the ambulance on the way to the hospital so that the ambulance crew could administer intracardiac adrenaline to her, although this procedure is now debatable, and no more recommended by the United Kingdom Resuscitation Council. Shouldn’t first-aiders/first responders, paramedics, ambulance crew etc. in this country be similarly trained up to that standard as well?
Alternative first aid medicine:
Interestingly, in one form of alternative medicine (reflexology), the modality of treatment is to massage certain pressure zones on the soles of both feet. This seems to elicit a response by sending pulses to the brain, which in turn stimulates the sympathetic autonomic nervous system* (see foot-note for explanation) to force the bronchi to relax, simultaneously sending another set of impulses to the adrenal glands (lies superior to the kidneys) to excite the cortex (outer layer) of this gland to release all the corticosteroidal hormones, and also the medulla (inner layer) of the adrenal gland to discharge the much needed adrenaline and noradrenaline into the blood. Noradrenaline is also produced by the sympathetic ganglia other than from the medulla. These natural hormones produced by the body are exactly the same drugs (other than antihistamines) a doctor would have injected to counteract the anaphylaxis. I know of at least two cases where patients recovered (at least for bronchial asthma) uneventfully through this procedure without any further intervention. This drug-free approach seems very interesting. However a larger population study would be needed for statistical analysis on this harmless modality if conventional first-aid becomes ineffective in certain situations.
Coffee as a bronchodilator:
Let us now move on to consider another very safe and common bronchodilator. And that’s just plain black coffee. Numerous clinical studies and I shall quote just two (6, 7), have shown that coffee has the same therapeutic value as aminophylline, a bronchodilating agent. Aminophylline is given at a dose of 250-350 mg i.v. over 15 minutes to keep the bronchioles patent in asthmatic patients (3). This dose is equivalent to 600 mg of caffeine which is found in two cups of very strong black coffee (no milk please. Cow’s milk protein can trigger off an allergic reaction, and makes the problem worse). Coffee contains these two drugs – aminophylline and theophylline, already present naturally in it. Both these agents are used as powerful bronchodialators in prolonged and severe asthma (status asthmaticus). Even if the aminophylline and theophylline are removed from coffee, the caffeine in the coffee itself will metabolically breakdown into these two natural drugs and make them available to the body.
Alternatives with similar mode of action:
Consider these mechanisms as some of the possibilities in first-aid for bronchospasm and angiooedema as features of anaphylaxis? I do not know the answers with certainty myself, but I am thinking of them as possibilities in the light of our scientific knowledge, and the work done by others (3,6,7). Again, questions we must seriously ask are: Can some of these harmless naturally occurring substances which show similar and promising pharmacological actions as the more powerful drugs, be used in the interim before medical intervention with more powerful and faster acting agents becomes accessible to the victim? Can they be given in the first place? Should they be given? Will they be effective? Of course one must remember not to feed anything through the mouth, not even a teaspoonful of water (except wetting the lips with water) if the patient is unconscious or unable to swallow. Once in the hospital, all medication or fluid may have to be given parenterally (non-oral route) via vascular access. For the moment the priority for the first-aider is merely to secure the airway, ensure breathing, and circulation, and transport the victim as early as possible to a hospital. Good luck. Hope you wont meet such a casualty. It can be very eventful.
Foot-note:
By the way, for those not familiar with the meaning of autonomic nervous system, very briefly, the autonomic nervous system is part of the central nervous system, and is made up of ganglia and fibres. It is divided into two major components – the sympathetic and the parasympathetic nervous systems. The functions of both systems are to control involuntary activities involving the smooth muscles, such as those responsible for respiration, heart beat, digestion, pupil size, etc. The sympathetic and parasympathetic nervous systems work in opposite action to one another. One stimulates, and the other inhibits the action.
Physiology of the 10th cranial nerve:
For example, the sympathetic nerve accelerates the heart beat, while the parasympathetic slows it down. The 10th cranial nerve is the vagus nerve, and is a parasympathetic nerve that controls and slows down the heart-rate. The nerve that accelerates the heart is called the accelerator or augmentor sympathetic nerve. If the vagus nerve is stimulated, it will slow down the heart rate to the extent of inducing a cardiac arrest (similar to giving excessive potassium). But if the stimulus is continuously applied, the heart will escape this vagal restraint, and commence to beat again (‘vagal escape of the heart’), with the first few ventricular contractions being exceptionally forceful. I must say nature is very kind to us to ensure we continue to survive.
Vagal escape:
If the vagus nerve is cut, or temporary paralyzed by a full dose of atropine (a drug with parasympatholytic action), the heart rate will be doubled (150 –180 beats per minute). Just for information sake, the vagus nerve is not there just to control the heart. After it emerges from the medulla oblongata (part of the brain stem), this longest cranial nerve starts to supply branches to the larynx, pharynx, trachea, heart, lungs, and most of the digestive system, and controls all of them.
References:
1. Yadav, M., Formerly, Professor of Immunology, University of Malaya, currently Consultant Immunologist and Allergist. Penicillin and Anaphylaxis. A Personal Communication. Nov. 1998.
2. Feng, P.H., Fock, K.M., Eng, Philip. Handbook of Acute Medicine (5th edition, 1992), Pages 76-78. APAC Publishers, Singapore.
3. Robinson, R., Stott, Robin. Medical Emergencies, Diagnosis and Management (6th edition, 1994), 345-346. CBS Publishers & Distributors, Delhi, India
4. Bochner B. et al. (1991). Anaphylaxis. N. Engl. J. Med. 324:1785.
5. Brueton M. et al. (1991). Management of anaphylaxis. Hospital Update May, page 386.
6. Becker, A.B., et al. The Bronchodilator Effects and Pharmacokinetics of Caffeine in Asthma.” New Engl. J. Med. (March 22, 1984). 310 (12): 743-746.
7. Gong. H., Jr., et al. Bronchodilator Effects of Caffeine in Coffee. A Dose-Response Study of Asthmatic Subjects.” Chest (March, 1986), 89(3): 335-342.
8. Brady Emergency Care, Grant, H.D, et al. (7th edition, 1995). Prentice-Hall International (UK) Ltd. London.
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