Stillbirth and an excess of amniotic fluid (polyhydramnios) are common during pregnancy with a HLS-affected foetus, with cases of up to 8 litres cited compared to the normal 1 litre. Less common symptoms such as abnormally small eyes and a broad nose are also possible. Cause
Genetic
HLS is caused by a genetic missense mutation of the HYLS1 gene, encoding for Hydrolethalus syndrome protein 1, on chromosome 11; a single base change to the amino acid sequence for HYLS1 in exon 6 involves the replacement of aspartic acid 211 with glycine (D211G) in the polypeptide chain. Exon 6 is the only protein coding exon in HYLS1; proper functioning of exons 1-5 ensures regulation and expression of the entire protein. HLS is an autosomal recessive syndrome; development is only possible if both parents carry the defective gene, and in that instance, the risk of the foetus developing the syndrome is 25%. HLS is a member of the Finnish disease heritage, with incidences more common in Finland than the rest of the world; roughly 1 in 20,000 developing foetuses are affected in Finland. Rare cases in other regions have also been documented, often with less severe phenotypes as a result of allele variability across countries, allowing survival of affected offspring for up to several months. Individuals of Finnish descent are advised to undergo genetic testing before attempting to conceive.Prior to the discovery of HLS, the HYLS1 gene was unknown, and similar genes within humans have not been identified.
Some of the symptoms of increased cholinergic stimulation include:

Salivation: stimulation of the salivary glands
Lacrimation: stimulation of the lacrimal glands (tearing)
Urination: relaxation of the internal sphincter muscle of urethra, and contraction of the detrusor muscles
Defecation
Gastrointestinal distress:     Smooth muscle tone changes causing gastrointestinal problems, including cramping
Emesis: Vomiting
Miosis constriction of the pupils of the eye via stimulation of the pupillary constrictor muscles
Muscle spasm: stimulation of skeletal muscle (due to nicotinic acetylcholine receptor stimulation)

Cause
Cholinergic crisis, sometimes known by the mnemonic "SLUDGE syndrome" ( Salivation, Lacrimation, Urination, Defecation, Gastrointestinal distress and Emesis), can be a consequence of:

Contamination with - or excessive exposure to - certain chemicals including:
nerve agents, (e.g. sarin, VX, Novichok agents). organophosphorus insecticides (e.g. parathion, aldicarb)
nicotine poisoning can be thought of as a subset of cholinergic crisis, as it also involves excessive parasympathetic stimulation. Ingestion of certain poisonous fungi (particularly the muscarine-containing members of the genera Amanita, Inocybe and Clitocybe). In medicine, this is seen in patients with myasthenia gravis who take too high a dose of medications such as cholinesterase inhibitors, or seen following general anaesthesia, when too high a dose of a cholinesterase inhibitor drug is given to reverse surgical muscle paralysis. Treatment
Some elements of the cholinergic crisis can be reversed with antimuscarinic drugs like atropine or diphenhydramine, but the most dangerous effect - respiratory depression, cannot. The neuromuscular junction, where the brain communicates with muscles (like the diaphragm, the main breathing muscle), works by acetylcholine activating nicotinic acetylcholine receptors and leading to muscle contraction.